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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Speer6-ps1Tg(Alb-cre)21Mgn
transgene insertion 21, Mark A Magnuson
MGI:2176228
Summary 207 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
cn1
Abcc6tm1c(EUCOMM)Wtsi/Abcc6tm1c(EUCOMM)Wtsi
Speer6-ps1Tg(Alb-cre)21Mgn/?
B6.Cg-Abcc6tm1c(EUCOMM)Wtsi Speer6-ps1Tg(Alb-cre)21Mgn MGI:6241503
cn2
Abcc6tm1c(EUCOMM)Wtsi/Abcc6tm1c(EUCOMM)Wtsi
Speer6-ps1Tg(Alb-cre)21Mgn/?
Tg(Cdx1-cre)23Kem/?
B6.Cg-Abcc6tm1c(EUCOMM)Wtsi Speer6-ps1Tg(Alb-cre)21Mgn Tg(Cdx1-cre)23Kem MGI:6241505
cn3
Adh5tm1.1Llli/Adh5tm1.1Llli
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
B6.Cg-Adh5tm1.1Llli Speer6-ps1Tg(Alb-cre)21Mgn MGI:5049927
cn4
Ahrtm3.1Bra/Ahrtm3.1Bra
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
B6.Cg-Ahrtm3.1Bra Speer6-ps1Tg(Alb-cre)21Mgn MGI:3613531
cn5
Abcc6tm1c(EUCOMM)Wtsi/Abcc6tm1c(EUCOMM)Wtsi
E2f1Tg(Wnt1-cre)2Sor/?
Speer6-ps1Tg(Alb-cre)21Mgn/?
B6.Cg-E2f1Tg(Wnt1-cre)2Sor Abcc6tm1c(EUCOMM)Wtsi Speer6-ps1Tg(Alb-cre)21Mgn MGI:6241501
cn6
Ggcxtm1Sino/Ggcx+
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
B6.Cg-Ggcxtm1Sino Speer6-ps1Tg(Alb-cre)21Mgn MGI:5662241
cn7
Ggcxtm1Sino/Ggcxtm1Sino
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
B6.Cg-Ggcxtm1Sino Speer6-ps1Tg(Alb-cre)21Mgn MGI:5662240
cn8
Hmgcltm2Gam/Hmgcltm2Gam
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
B6.Cg-Hmgcltm2Gam Speer6-ps1Tg(Alb-cre)21Mgn MGI:5538628
cn9
Hs2st1tm1.1Je/Hs2st1tm1.1Je
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
B6.Cg-Hs2st1tm1.1Je Speer6-ps1Tg(Alb-cre)21Mgn MGI:4439271
cn10
Mob1atm1.1Asuz/Mob1atm1.1Asuz
Mob1bGt(CC0690)Wtsi/Mob1bGt(CC0690)Wtsi
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
B6.Cg-Mob1bGt(CC0690)Wtsi Mob1atm1.1Asuz Speer6-ps1Tg(Alb-cre)21Mgn MGI:5897809
cn11
Scarb1tm1Thh/Scarb1tm1Thh
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
B6.Cg-Scarb1tm1Thh Speer6-ps1Tg(Alb-cre)21Mgn MGI:3697677
cn12
Ahrb-1/Ahrb-1
Aiptm2.1Bra/Aiptm2.1Bra
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
B6.Cg-Speer6-ps1Tg(Alb-cre)21Mgn Aiptm2.1Bra MGI:4867849
cn13
Naa40tm1Qwzh/Naa40tm1Qwzh
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
B6.Cg-Speer6-ps1Tg(Alb-cre)21Mgn Naa40tm1Qwzh MGI:5317915
cn14
Scd1tm2Ntam/Scd1tm2Ntam
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
B6.Cg-Speer6-ps1Tg(Alb-cre)21Mgn Scd1tm2Ntam MGI:3773310
cn15
Abcb7tm1Mdf/Y
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
either: B6.Cg-Speer6-ps1Tg(Alb-cre)21Mgn Abcb7tm1Mdf or (involves: 129S4/SvJae * 129S6/SvEvTac * C57BL/6 * DBA) MGI:3629066
cn16
Cav1tm1Pesch/Cav1tm1Pesch
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
FVB.Cg-Cav1tm1Pesch Speer6-ps1Tg(Alb-cre)21Mgn MGI:5316849
cn17
Stk3tm1Jav/Stk3tm1Jav
Stk4Gt(AJ0315)Wtsi/Stk4Gt(AJ0315)Wtsi
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129 * 129P2/OlaHsd * C57BL/6 * DBA MGI:5824005
cn18
Arnttm1Bra/Arnttm1Bra
Vhltm1Jae/Vhltm1Jae
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129 * BALB/c * C57BL/6 * DBA MGI:3621473
cn19
Hif1atm3Rsjo/Hif1atm3Rsjo
Vhltm1Jae/Vhltm1Jae
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129 * BALB/c * C57BL/6 * DBA MGI:3621471
cn20
Stk3tm1Jav/Stk3tm1Jav
Stk4Gt(AJ0315)Wtsi/Stk4Gt(AJ0315)Wtsi
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129 * C57BL/6 MGI:4411991
cn21
Gfertm1.1Crg/Gfertm1.1Crg
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129 * C57BL/6 * DBA MGI:5762654
cn22
Ppargc1atm2Brsp/Ppargc1atm2Brsp
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129 * C57BL/6 * DBA MGI:3694896
cn23
Ccn1tm3.1Lfl/Ccn1tm3.1Lfl
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129 * C57BL/6 * DBA MGI:5529807
cn24
Hif1antm1.1Rsjo/Hif1antm1.1Rsjo
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129 * C57BL/6 * DBA MGI:4459910
cn25
Nus1tm1.1Qrm/Nus1tm1.1Qrm
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129 * C57BL/6 * DBA * SJL MGI:6106900
cn26
Cdk1tm2.1Kald/Cdk1tm2.1Kald
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129 * C57BL/6 * DBA * SJL MGI:5318109
cn27
Nr1h3tm1Djm/Nr1h3tm1Djm
Nus1tm1.1Qrm/Nus1tm1.1Qrm
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129 * C57BL/6 * DBA * SJL MGI:6106901
cn28
Ptpn11tm1Gsf/Ptpn11tm1Gsf
Stat3tm1Vpo/Stat3tm1Vpo
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * C57BL/6 * DBA MGI:5009547
cn29
Ccn2tm1.1Alea/Ccn2tm1.1Alea
Mob1atm1.1Asuz/Mob1atm1.1Asuz
Mob1bGt(CC0690)Wtsi/Mob1bGt(CC0690)Wtsi
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6 * DBA MGI:5897813
cn30
Irs1tm2Tka/Irs1tm2Tka
Irs2tm2Tka/Irs2tm2Tka
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * DBA MGI:3805348
cn31
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53+
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * DBA MGI:5428898
cn32
Atp8b1tm1Nbf/Atp8b1tm1Nbf
Portm1Wolf/Portm1Wolf
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * DBA MGI:5618808
cn33
Krastm4Tyj/Kras+
Ptentm2Mak/Pten+
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * DBA MGI:6256732
cn34
Krastm4Tyj/Kras+
Ptentm2Mak/Ptentm2Mak
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * DBA MGI:6256730
cn35
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm1Brn
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * DBA MGI:5428907
cn36
Akt2tm1.1Mbb/Akt2tm1.1Mbb
Ptentm1Hwu/Ptentm1Hwu
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * DBA MGI:4838529
cn37
Krastm4Tyj/Krastm4Tyj
Yap1tm1.1Dupa/Yap1tm1.1Dupa
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * DBA MGI:4819844
cn38
Mettm1Sst/Mettm1Sst
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129P2/OlaHsd * C57BL/6 MGI:3041261
cn39
Ptentm2Mak/Ptentm2Mak
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129P2/OlaHsd * C57BL/6 * C57BL/6J * DBA MGI:5702658
cn40
Mob1atm1.1Asuz/Mob1atm1.1Asuz
Mob1bGt(CC0690)Wtsi/Mob1bGt(CC0690)Wtsi
Yap1tm1c(KOMP)Mbp/Yap1tm1c(KOMP)Mbp
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129P2/OlaHsd * C57BL/6 * C57BL/6N * DBA MGI:5897815
cn41
Foxa2tm1Khk/Foxa2tm1Khk
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129P2/OlaHsd * C57BL/6 * CD-1 * DBA MGI:2177363
cn42
Rr27tm2Msb/Rr27+
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129P2/OlaHsd * C57BL/6 * DBA MGI:3620114
cn43
Keap1tm1Mym/Keap1tm2Mym
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129P2/OlaHsd * C57BL/6 * DBA MGI:3620636
cn44
Irs1tm2Tka/Irs1tm2Tka
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129P2/OlaHsd * C57BL/6 * DBA MGI:3805350
cn45
Ptentm2Mak/Ptentm2Mak
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129P2/OlaHsd * C57BL/6 * DBA MGI:3806986
cn46
Cyb5atm1Wolf/Cyb5atm1Wolf
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129P2/OlaHsd * C57BL/6 * DBA MGI:3826674
cn47
Acsl1tm1Rcol/Acsl1tm1Rcol
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129P2/OlaHsd * C57BL/6 * DBA MGI:4417849
cn48
Yap1tm1.1Dupa/Yap1tm1.1Dupa
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129P2/OlaHsd * C57BL/6 * DBA MGI:4819841
cn49
Nf2tm2Gth/Nf2tm2Gth
Yap1tm1.1Dupa/Yap1tm1.1Dupa
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129P2/OlaHsd * C57BL/6 * DBA MGI:4819842
cn50
Nf2tm2Gth/Nf2tm2Gth
Yap1tm1.1Dupa/Yap1+
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129P2/OlaHsd * C57BL/6 * DBA MGI:4819843
cn51
Nf2tm2Gth/Nf2tm2Gth
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129P2/OlaHsd * C57BL/6 * DBA MGI:4819845
cn52
Apoetm1Unc/Apoetm1Unc
Smarcd1tm1.1Jddl/Smarcd1tm1.1Jddl
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129P2/OlaHsd * C57BL/6 * DBA MGI:5912277
cn53
Stat3tm1Vpo/Stat3tm1Vpo
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129P2/OlaHsd * C57BL/6 * DBA MGI:5009548
cn54
Mob1atm1.1Asuz/Mob1atm1.1Asuz
Mob1bGt(CC0690)Wtsi/Mob1bGt(CC0690)Wtsi
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
Tgfbr2tm1Roes/Tgfbr2tm1Roes
involves: 129P2/OlaHsd * C57BL/6 * DBA MGI:5897816
cn55
Mob1atm1.1Asuz/Mob1atm1.1Asuz
Mob1bGt(CC0690)Wtsi/Mob1bGt(CC0690)Wtsi
Wwtr1tm1Hku/Wwtr1tm1Hku
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129P2/OlaHsd * C57BL/6 * DBA MGI:5897811
cn56
Hsd11b1tm1Ggla/Hsd11b1tm1Ggla
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129P2/OlaHsd * C57BL/6 * DBA MGI:5444453
cn57
Hmgb1tm1.1Ttg/Hmgb1tm1.1Ttg
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129P2/OlaHsd * C57BL/6 * DBA MGI:5563542
cn58
Portm1Wolf/Portm1Wolf
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129P2/OlaHsd * C57BL/6 * DBA/2 MGI:2656922
cn59
Map3k7tm1Aki/Map3k7tm1Aki
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129P2/OlaHsd * C57BL/6 * DBA/2 MGI:4461042
cn60
Portm2Wolf/Portm1Wolf
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129P2/OlaHsd * C57BL/6 * DBA/2 MGI:2656921
cn61
Abcb4tm1Bor/Abcb4tm1Bor
Portm1Wolf/Portm1Wolf
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129P2/OlaHsd * C57BL/6 * DBA * FVB/N MGI:5618809
cn62
Abhd5tm1.1Lqyu/Abhd5tm1.1Lqyu
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129S1/Sv * 129S4/SvJaeSor * 129X1/SvJ * C57BL/6 * DBA MGI:5523090
cn63
Pdss2tm1Dalg/Pdss2tm1Dalg
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 MGI:3805708
cn64
Gab1tm1Gsf/Gab1tm1Gsf
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 MGI:3578950
cn65
Mtch2tm2Atgr/Mtch2tm2.1Atgr
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * DBA MGI:5566667
cn66
Irs1tm1Mfw/Irs1tm1Mfw
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * DBA MGI:3805308
cn67
Ptpn11tm1Gsf/Ptpn11tm1Gsf
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * DBA MGI:5009546
cn68
Ern1tm1Rjk/Ern1tm2.1Rjk
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * DBA MGI:4949418
cn69
Mir122tm1Kgh/Mir122+
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * DBA MGI:5448536
cn70
Ndst1tm1Je/Ndst1tm1Je
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * DBA MGI:4439272
cn71
Pex5tm1Pec/Pex5tm1Pec
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * DBA MGI:3851810
cn72
Adartm1Knk/Adartm1Knk
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * DBA MGI:3032498
cn73
Mir122tm1Kgh/Mir122tm1Kgh
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * DBA MGI:5448537
cn74
Ei24tm1Hzha/Ei24tm1Hzha
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * DBA MGI:5475096
cn75
Pcsk9tm1.1Prat/Pcsk9tm1.1Prat
Speer6-ps1Tg(Alb-cre)21Mgn/?
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * DBA MGI:4943540
cn76
Irs2tm2Mfw/Irs2tm2Mfw
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * DBA MGI:3805307
cn77
Irs1tm1Mfw/Irs1tm1Mfw
Irs2tm2Mfw/Irs2tm2Mfw
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * DBA MGI:3805306
cn78
Foxo1tm1Rdp/Foxo1tm1Rdp
Irs1tm1Mfw/Irs1tm1Mfw
Irs2tm2Mfw/Irs2tm2Mfw
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * DBA * FVB MGI:3805304
cn79
Irs1tm2.1Mfw/Irs1tm2.1Mfw
Irs2tm2Mfw/Irs2tm2Mfw
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129S1/Sv * 129X1/SvJ * C57BL/6J * DBA * FVB/N MGI:4430358
cn80
Irs1tm1Mfw/Irs1tm2.1Mfw
Irs2tm2Mfw/Irs2tm2Mfw
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129S1/Sv * 129X1/SvJ * C57BL/6J * DBA * FVB/N MGI:4430356
cn81
Irs1tm1Mfw/Irs1+
Irs2tm2Mfw/Irs2tm2Mfw
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129S1/Sv * 129X1/SvJ * C57BL/6J * DBA * FVB/N MGI:4430357
cn82
Portm1Ding/Por+
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129S1/Sv * C57BL/6 * DBA MGI:3704087
cn83
Portm1Ding/Portm1Ding
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129S1/Sv * C57BL/6 * DBA MGI:2668453
cn84
Notch2tm3Grid/Notch2tm3.1Grid
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129S1/Sv * C57BL/6 * DBA MGI:3778811
cn85
Aqp11tm1.1Nlsn/Aqp11tm1.1Nlsn
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129S1/Sv * C57BL/6 * DBA MGI:5485021
cn86
Notch2tm2Grid/Notch2tm3Grid
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129S1/Sv * C57BL/6 * DBA MGI:3778812
cn87
Foxo1tm1Rdp/Foxo1tm1Rdp
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129S1/Sv * C57BL/6 * DBA * FVB MGI:3805303
cn88
Pros1tm1Grl/Pros1tm1Grl
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129S1/SvImJ * C57BL/6 * DBA MGI:5499118
cn89
Slc25a4tm2Dwa/Slc25a4tm2Dwa
Slc25a5tm1Dwa/Y
Speer6-ps1Tg(Alb-cre)21Mgn/?
involves: 129S4/SvJae MGI:3036352
cn90
Ncor1tm1Anh/Ncor1tm1Anh
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129S4/SvJae * 129S4/SvJaeSor * C57BL/6 * DBA MGI:3821875
cn91
Vhltm1Jae/Vhltm1Jae
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129S4/SvJae * BALB/c * C57BL/6 * DBA MGI:2176966
cn92
Pnpla2tm1Gam/Pnpla2tm1Gam
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129S4/SvJae * C57BL/6 * C57BL/6J * DBA MGI:5427456
cn93
Fbxw7tm1Iken/Fbxw7+
Krastm4Tyj/Kras+
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129S4/SvJae * C57BL/6 * C57BL/6N * DBA MGI:6157295
cn94
Fbxw7tm1Iken/Fbxw7tm1Iken
Krastm4Tyj/Kras+
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129S4/SvJae * C57BL/6 * C57BL/6N * DBA MGI:6157296
cn95
Ptentm1Hwu/Ptentm1Hwu
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129S4/SvJae * C57BL/6 * DBA MGI:4829790
cn96
Rragatm2Dmsa/Rragatm2Dmsa
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129S4/SvJae * C57BL/6 * DBA MGI:6236292
cn97
Tsc1tm1Djk/Tsc1tm1Djk
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129S4/SvJae * C57BL/6 * DBA MGI:5009705
cn98
Krastm4Tyj/Kras+
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129S4/SvJae * C57BL/6 * DBA MGI:5428897
cn99
Vhltm1Jae/Vhltm1Jae
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129S4/SvJae * C57BL/6 * DBA MGI:3832405
cn100
Irs2tm2Tka/Irs2tm2Tka
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129S4/SvJae * C57BL/6 * DBA MGI:3805349
cn101
Insrtm1Khn/Insrtm1Khn
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
Tg(Ins2-cre)25Mgn/0
involves: 129S4/SvJae * C57BL/6 * DBA/2 MGI:3775382
cn102
Ptpn1tm2Bbk/Ptpn1tm2Bbk
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129S4/SvJae * C57BL/6 * DBA/2 MGI:3664093
cn103
Insrtm1Khn/Insrtm1Khn
Pdx1tm1Ted/Pdx1+
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129S4/SvJae * C57BL/6 * DBA/2 MGI:3583116
cn104
Insrtm1Khn/Insrtm1Khn
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129S4/SvJae * C57BL/6 * DBA/2 MGI:3775385
cn105
Gt(ROSA)26Sortm2(sb11)Njen/Gt(ROSA)26Sor+
Trp53tm3Tyj/Trp53+
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
TgTn(sb-T2/Onc)68Dla/0
involves: 129S4/SvJae * C57BL/6 * DBA/2 * FVB/N MGI:3839859
cn106
Sephs1tm1.1Dhat/Sephs1tm1.1Dhat
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129S4/SvJae * C57BL/6J MGI:6189551
cn107
Insrtm1Khn/Insrtm1Khn
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129S4/SvJae * C57BL/6J * DBA/2 * FVB MGI:3039262
cn108
Zbtb20tm1Wpjz/Zbtb20tm1Wpjz
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129S4/SvJae * C57BL * C57BL/6 * DBA MGI:3812018
cn109
Slc25a37tm1.1Kapl/Slc25a37tm1.2Kapl
Speer6-ps1Tg(Alb-cre)21Mgn/?
involves: 129S4/SvJaeSor * 129S6/SvEvTac * C57BL/6J * C57BL/6NCr * DBA MGI:5014820
cn110
Ghrtm1.1Masp/Ghrtm1.1Masp
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129S4/SvJaeSor * C57BL/6 * DBA MGI:4359908
cn111
Cdk5rap3tm1c(EUCOMM)Hmgu/Cdk5rap3tm1c(EUCOMM)Hmgu
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129S4/SvJaeSor * C57BL/6N * DBA MGI:6295913
cn112
Pck1tm1.1Mgn/Pck1tm1.1Mgn
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129S6/SvEvTac MGI:3029211
cn113
Abca1tm1Jp/Abca1tm1Jp
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129S6/SvEvTac * B6.Cg-Tg(Alb-cre)21Mgn/J MGI:3578113
cn114
Abca1tm1Jp/Abca1+
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129S6/SvEvTac * B6.Cg-Tg(Alb-cre)21Mgn/J MGI:3578114
cn115
Gt(ROSA)26Sortm4(HIF2A*)Kael/Gt(ROSA)26Sor+
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129S6/SvEvTac * BALB/c * C57BL/6 * DBA MGI:3832403
cn116
Gt(ROSA)26Sortm3(HIF1A*)Kael/Gt(ROSA)26Sortm4(HIF2A*)Kael
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129S6/SvEvTac * BALB/c * C57BL/6 * DBA MGI:3832404
cn117
Gt(ROSA)26Sortm3(HIF1A*)Kael/Gt(ROSA)26Sor+
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129S6/SvEvTac * BALB/c * C57BL/6 * DBA MGI:3832402
cn118
Hjvtm1Kpan/Hjvtm1Kpan
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129S6/SvEvTac * C57BL/6 MGI:5792902
cn119
Lamp2tm1Amcu/Y
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129S6/SvEvTac * C57BL/6 * C57BL/6J MGI:5691397
cn120
Il7tm2.1Iku/Il7tm2.1Iku
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129S6/SvEvTac * C57BL/6 * C57BL/6J * DBA MGI:5461227
cn121
Gys2tm1.1Pro/Gys2tm1.1Pro
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129S6/SvEvTac * C57BL/6 * C57BL/6J * DBA MGI:4462847
cn122
Sav1tm1.1Rjo/Sav1tm1.1Rjo
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129S6/SvEvTac * C57BL/6 * CD-1 * DBA * SJL MGI:4430548
cn123
Stk3tm1.1Rjo/Stk3tm1.1Rjo
Stk4tm1.1Rjo/Stk4tm1.1Rjo
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129S6/SvEvTac * C57BL/6 * CD-1 * DBA * SJL MGI:4430567
cn124
Srebf2tm1Jdh/Srebf2tm1Jdh
Speer6-ps1Tg(Alb-cre)21Mgn/?
involves: 129S6/SvEvTac * C57BL/6 * DBA MGI:5908398
cn125
Abca1tm1Jp/Abca1tm1Jp
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129S6/SvEvTac * C57BL/6 * DBA MGI:4358982
cn126
Hdac3tm1Swh/Hdac3tm1.1Swh
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129S6/SvEvTac * C57BL/6 * DBA MGI:3795939
cn127
Gclctm1Tdal/Gclctm1Tdal
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129S6/SvEvTac * C57BL/6 * DBA MGI:5519060
cn128
Gaktm2Legr/Gaktm2Legr
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129S6/SvEvTac * C57BL/6 * DBA MGI:5305778
cn129
Hs6st1tm1Wvc/Hs6st1tm1Wvc
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129S6/SvEvTac * C57BL/6 * DBA MGI:4439273
cn130
Gcktm1.1Mgn/Gcktm1.1Mgn
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129S6/SvEvTac * C57BL/6 * DBA/2 MGI:3603013
cn131
Chrm3tm2.1Jwe/Chrm3tm2.1Jwe
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129S6/SvEvTac * C57BL/6 * DBA * FVB/N MGI:4438748
cn132
Abca1tm1Jp/Abca1tm1Jp
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
Tg(Vil1-cre)997Gum/0
involves: 129S6/SvEvTac * C57BL/6 * DBA * SJL MGI:4358977
cn133
Coq7tm1Hek/Coq7tm2Hek
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129S6/SvEvTac * C57BL/6NTac MGI:5532534
cn134
Acacatm2Sjw/Acacatm2Sjw
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129S7/SvEvBrd * C57BL/6J * FVB MGI:3641135
cn135
Soat2tm1.1Llr/Soat2tm1.1Llr
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129S/SvEv * 129S4/SvJaeSor * C57BL/6 * DBA MGI:5426955
cn136
Nr5a2tm1Sakl/Nr5a2tm1Sakl
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129S/SvEv * 129S4/SvJaeSor * C57BL/6 * DBA MGI:3797770
cn137
Tmem30atm1.1Xjz/Tmem30atm1.1Xjz
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129S/SvEv * 129S4/SvJaeSor * C57BL/6J * DBA MGI:6119462
cn138
Ldlrtm1Her/Ldlrtm1Her
Nr1h3tm1.1Djm/Nr1h3tm1.1Djm
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129S/SvEv * 129S7/SvEvBrd * C57BL/6 * DBA MGI:5427004
cn139
Nr0b2tm1Mjev/Nr0b2tm1Mjev
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129S/SvEvBrd * C57BL/6 * DBA MGI:3847955
cn140
Rptortm1.1Dmsa/Rptortm1.1Dmsa
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129S/SvEv * C57BL/6 * DBA MGI:4879104
cn141
Nr1h3tm1.1Djm/Nr1h3tm1.1Djm
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129S/SvEv * C57BL/6 * DBA MGI:5427002
cn142
Commd1tm2.1Bvds/Commd1tm2.1Bvds
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129S/SvEv * C57BL/6 * DBA * SJL MGI:5315714
cn143
Smad2tm1.1Epb/Smad2tm1.1Epb
Smad3tm1Cxd/Smad3tm1Cxd
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129/Sv * 129S6/SvEvTac * C57BL/6 * DBA * SJL MGI:3703883
cn144
Ldlrtm1Her/Ldlrtm1Her
Nr5a2tm1Sjns/Nr5a2tm1Sjns
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129/Sv * 129S7/SvEvBrd * C57BL/6 * C57BL/6J * DBA MGI:5607406
cn145
Igf2rtm1Rlj/Igf2r+
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129/Sv * C57BL/6 * DBA MGI:3795373
cn146
Raratm3Ipc/Raratm3Ipc
Speer6-ps1Tg(Alb-cre)21Mgn/?
Trim24tm1Los/Trim24tm1Los
involves: 129/Sv * C57BL/6 * DBA * SJL MGI:3772096
cn147
Raratm3Ipc/Rara+
Speer6-ps1Tg(Alb-cre)21Mgn/?
Trim24tm1Los/Trim24tm1Los
involves: 129/Sv * C57BL/6 * DBA * SJL MGI:3772097
cn148
Smad2tm1.1Epb/Smad2tm1.1Epb
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129/Sv * C57BL/6 * DBA * SJL MGI:3703880
cn149
Ptpn11tm3Bgn/Ptpn11tm3Bgn
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129X1/SvJ * C57BL/6 * C57BL/6J * DBA MGI:4868455
cn150
Fasntm1Sem/Fasntm1Sem
Speer6-ps1Tg(Alb-cre)21Mgn/?
involves: 129X1/SvJ * C57BL/6 * DBA MGI:3765082
cn151
Hnf1atm1.1Ylee/Hnf1atm2Ylee
Speer6-ps1Tg(Alb-cre)21Mgn/?
involves: 129X1/SvJ * C57BL/6 * DBA MGI:3818297
cn152
Foxm1tm1Rhc/Foxm1tm1Rhc
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129X1/SvJ * C57BL/6 * DBA MGI:3522661
cn153
Nfe2l1tm1Jefc/Nfe2l1tm1Ywk
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129X1/SvJ * C57BL/6J MGI:3575312
cn154
Prkacatm3Gsm/Prkacatm3Gsm
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129X1/SvJ * C57BL/6J MGI:3615115
cn155
Gt(ROSA)26Sortm2Bet/Gt(ROSA)26Sortm2Bet
Speer6-ps1Tg(Alb-cre)21Mgn/?
involves: BALB/c * C57BL/6 * DBA MGI:5086106
cn156
Srsf3tm1Pjln/Srsf3tm1Pjln
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: BALB/c * C57BL/6 * DBA MGI:5605688
cn157
Cluhtm1.1Eir/Cluhtm1.1Eir
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: BALB/cJ * C57BL/6 * DBA * SJL MGI:6119620
cn158
Lman1tm1c(KOMP)Wtsi/Lman1tm1c(KOMP)Wtsi
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: C57BL/6 * C57BL/6J * C57BL/6N MGI:5607591
cn159
Hmox1tm1.1Hes/Hmox1tm1.1Hes
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: C57BL/6 * C57BL/6J * C57BL/6N * DBA MGI:5660646
cn160
Mpc1tm1c(EUCOMM)Wtsi/Mpc1tm1c(EUCOMM)Wtsi
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: C57BL/6 * C57BL/6J * C57BL/6N * DBA MGI:5903311
cn161
Sirt3tm1.1Auw/Sirt3tm1.1Auw
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: C57BL/6 * C57BL/6J * DBA MGI:5556080
cn162
Glultm1.1Geno/Glultm1.1Geno
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: C57BL/6 * C57BL/6J * DBA MGI:5758759
cn163
Arntltm1.1Shbi/Arntltm1.1Shbi
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: C57BL/6 * C57BL/6J * DBA MGI:5613394
cn164
Pik3c3tm1c(EUCOMM)Wtsi/Pik3c3tm1c(EUCOMM)Wtsi
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
Tg(CAG-EGFP/Map1lc3b)53Nmz/0
involves: C57BL/6 * C57BL/6N * C57BL/6NCrj * DBA MGI:5427446
cn165
Faf2tm1Tfji/Faf2tm1Tfji
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: C57BL/6 * C57BL/6N * CBA * DBA MGI:5805372
cn166
Sco1tm1c(KOMP)Wtsi/Sco1tm1c(KOMP)Wtsi
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: C57BL/6 * C57BL/6N * DBA MGI:5758892
cn167
Fbxw7tm1Iken/Fbxw7tm1Iken
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: C57BL/6 * C57BL/6N * DBA MGI:6157293
cn168
Pik3c3tm1c(EUCOMM)Wtsi/Pik3c3tm1c(EUCOMM)Wtsi
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: C57BL/6 * C57BL/6N * DBA MGI:5427443
cn169
Secisbp2tm1c(EUCOMM)Wtsi/Secisbp2tm1c(EUCOMM)Wtsi
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: C57BL/6 * C57BL/6N * DBA MGI:5583958
cn170
Il6ratm1.1Drew/Il6ratm1.1Drew
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: C57BL/6 * C57BL/6N * SJL MGI:4456459
cn171
Lpcat3tm1c(EUCOMM)Wtsi/Lpcat3tm1c(EUCOMM)Wtsi
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: C57BL/6 * C57BL/6N * SJL MGI:5822858
cn172
Cul4atm1.1Pra/Cul4atm1.1Pra
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: C57BL/6 * C57BL/6NTac * DBA MGI:5003273
cn173
Stk3tm1.1Yy/Stk3tm1Yy
Stk4tm1.1Yy/Stk4tm1.1Yy
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: C57BL/6 * CBA * DBA MGI:4422187
cn174
Psmg1tm1.1Smta/Psmg1tm1.1Smta
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: C57BL/6 * CBA * DBA MGI:4820736
cn175
Psmd4tm2Smta/Psmd4tm2Smta
Speer6-ps1Tg(Alb-cre)21Mgn/?
involves: C57BL/6 * CBA * DBA MGI:3762177
cn176
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
Tspotm1.1Maf/Tspotm1.1Maf
involves: C57BL/6 * DBA MGI:5588662
cn177
Sqstm1tm2.1Jmos/Sqstm1tm2.1Jmos
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: C57BL/6 * DBA MGI:5487467
cn178
Pcyt2tm1.1Suja/Pcyt2tm1.1Suja
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: C57BL/6 * DBA MGI:4415291
cn179
Creg1em1Yal/Creg1em1Yal
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: C57BL/6 * DBA MGI:6196883
cn180
Portm3Ding/Portm3Ding
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: C57BL/6 * DBA MGI:4457494
cn181
Ddit3tm1.1Irt/Ddit3tm1.1Irt
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
Tg(Mup3-Plau)350-2Eps/?
involves: C57BL/6 * DBA MGI:5781097
cn182
Sav1tm2.1Dlim/Sav1tm2.1Dlim
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: C57BL/6 * DBA MGI:4457497
cn183
Txniptm1Road/Txniptm1Road
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: C57BL/6 * DBA MGI:3809845
cn184
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
Trmutm1Tomik/Trmutm1Tomik
involves: C57BL/6 * DBA MGI:6108884
cn185
Pnpt1tm1Teit/Pnpt1tm1Teit
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: C57BL/6 * DBA MGI:4882058
cn186
Derl2tm1.1Hpl/Derl2tm1.1Hpl
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: C57BL/6 * DBA MGI:4947224
cn187
Ccl2tm1.1Pame/Ccl2tm1.1Pame
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: C57BL/6 * DBA MGI:4950282
cn188
Smarcd1tm1.1Jddl/Smarcd1tm1.1Jddl
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: C57BL/6 * DBA MGI:5912276
cn189
Selenoptm3.1Rfb/Selenoptm3.1Rfb
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: C57BL/6 * DBA MGI:5466370
cn190
Gcktm1Hrt/Gck+
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: C57BL/6 * DBA MGI:3618231
cn191
Fbxl5tm2.1Kei/Fbxl5tm2.1Kei
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: C57BL/6 * DBA MGI:5295292
cn192
Dio3tm1Dmst/Dio3tm1Dmst
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: C57BL/6 * DBA MGI:5770122
cn193
Klf14tm1.1Yec/Klf14tm1.1Yec
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: C57BL/6 * DBA MGI:5882068
cn194
Trnau1aptm2.1Usch/Trnau1aptm2.1Usch
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: C57BL/6 * DBA MGI:5825445
cn195
Cdo1tm1Mhst/Cdo1tm1Mhst
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: C57BL/6 * DBA MGI:5437229
cn196
Nfe2l1tm1Mym/Nfe2l1tm1Mym
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: C57BL/6 * DBA MGI:3828255
cn197
Agap2tm1Kye/Agap2tm1Kye
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: C57BL/6 * DBA/2 MGI:5284899
cn198
Gt(ROSA)26Sortm2(sb11)Njen/Gt(ROSA)26Sor+
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
TgTn(sb-T2/Onc)68Dla/0
involves: C57BL/6 * DBA/2 * FVB/N MGI:3839857
cn199
Dbitm2.1Smdp/Dbi+
Dbitm2.2Smdp/Dbi+
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: C57BL/6 * DBA * FVB/N MGI:5538740
cn200
Abcg5tm1.1Hobb/Abcg5tm1.1Hobb
Abcg8tm1.1Hobb/Abcg8tm1.1Hobb
Speer6-ps1Tg(Alb-cre)21Mgn/?
involves: C57BL/6 * DBA * SJL MGI:5607618
cn201
Gcgrtm2.1Mjch/Gcgrtm2.1Mjch
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: C57BL/6 * DBA * SJL MGI:5566824
cn202
Sec24ctm1c(EUCOMM)Wtsi/Sec24ctm1c(EUCOMM)Wtsi
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: C57BL/6 * DBA * SJL MGI:5896384
cn203
Blvratm1c(EUCOMM)Hmgu/Blvratm1c(EUCOMM)Hmgu
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: C57BL/6J * C57BL/6N MGI:5822918
cn204
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
Tg(CAG-CAT,-Creg1)#Yal/0
involves: C57BL/6J * DBA MGI:6196884
cn205
Clk2tm1.1Ppgr/Clk2tm1.1Ppgr
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: C57BL/6NTac * FVB/N MGI:5751747
cn206
Antxr2tm1.1Lepp/Antxr2tm1.1Lepp
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: C57BL/6 * SJL MGI:4353035
cx207
Hif1atm3Rsjo/Hif1atm3Rsjo
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1Tg(Alb-cre)21Mgn
B6.Cg-Hif1atm3Rsjo Speer6-ps1Tg(Alb-cre)21Mgn MGI:6275178


Genotype
MGI:6241503
cn1
Allelic
Composition
Abcc6tm1c(EUCOMM)Wtsi/Abcc6tm1c(EUCOMM)Wtsi
Speer6-ps1Tg(Alb-cre)21Mgn/?
Genetic
Background
B6.Cg-Abcc6tm1c(EUCOMM)Wtsi Speer6-ps1Tg(Alb-cre)21Mgn
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Abcc6tm1c(EUCOMM)Wtsi mutation (1 available); any Abcc6 mutation (45 available)
Speer6-ps1Tg(Alb-cre)21Mgn mutation (5 available); any Speer6-ps1 mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism

integument
• calcification of the fibrous capsule surrounding the muzzle vibrissae is not observed at 20 weeks of age, however, at one year of age, some calcification is present

growth/size/body

craniofacial




Genotype
MGI:6241505
cn2
Allelic
Composition
Abcc6tm1c(EUCOMM)Wtsi/Abcc6tm1c(EUCOMM)Wtsi
Speer6-ps1Tg(Alb-cre)21Mgn/?
Tg(Cdx1-cre)23Kem/?
Genetic
Background
B6.Cg-Abcc6tm1c(EUCOMM)Wtsi Speer6-ps1Tg(Alb-cre)21Mgn Tg(Cdx1-cre)23Kem
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Abcc6tm1c(EUCOMM)Wtsi mutation (1 available); any Abcc6 mutation (45 available)
Speer6-ps1Tg(Alb-cre)21Mgn mutation (5 available); any Speer6-ps1 mutation (2 available)
Tg(Cdx1-cre)23Kem mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism

integument
• calcification of the fibrous capsule surrounding the muzzle vibrissae is not observed at 20 weeks of age, however, at one year of age, some calcification is present

growth/size/body

craniofacial




Genotype
MGI:5049927
cn3
Allelic
Composition
Adh5tm1.1Llli/Adh5tm1.1Llli
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
Genetic
Background
B6.Cg-Adh5tm1.1Llli Speer6-ps1Tg(Alb-cre)21Mgn
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Adh5tm1.1Llli mutation (0 available); any Adh5 mutation (16 available)
Speer6-ps1Tg(Alb-cre)21Mgn mutation (5 available); any Speer6-ps1 mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• diethylnitrosamine (DEN)-challenged mice exhibit decreased survival compared with similarly treated wild-type mice
• LPS-challenged mice exhibit decreased survival compared with similarly treated wild-type mice

homeostasis/metabolism
• diethylnitrosamine (DEN)-challenged mice exhibit decreased survival compared with similarly treated wild-type mice

immune system
• LPS-challenged mice exhibit decreased survival compared with similarly treated wild-type mice




Genotype
MGI:3613531
cn4
Allelic
Composition
Ahrtm3.1Bra/Ahrtm3.1Bra
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
Genetic
Background
B6.Cg-Ahrtm3.1Bra Speer6-ps1Tg(Alb-cre)21Mgn
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ahrtm3.1Bra mutation (1 available); any Ahr mutation (76 available)
Speer6-ps1Tg(Alb-cre)21Mgn mutation (5 available); any Speer6-ps1 mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
N
• no defect in the closure of the ductus venosus is seen unlike in mice homozygous for Ahrtm3Bra

homeostasis/metabolism
• exposure to 100 ug 2,3,7,8-tetrachlorodibenzo-p-dioxin failed to induce hepatomegaly, or Cyp1a2 expression, only weakly induced Cyp1a1 expression, partially induced Cyp1b1 expression, and resulted in significantly less liver damage compared to homozygous mice lacking the cre transgene
• however, exposure to 100 ug 2,3,7,8-tetrachlorodibenzo-p-dioxin did induce thymic involution similar to homozygous mice lacking the cre transgene




Genotype
MGI:6241501
cn5
Allelic
Composition
Abcc6tm1c(EUCOMM)Wtsi/Abcc6tm1c(EUCOMM)Wtsi
E2f1Tg(Wnt1-cre)2Sor/?
Speer6-ps1Tg(Alb-cre)21Mgn/?
Genetic
Background
B6.Cg-E2f1Tg(Wnt1-cre)2Sor Abcc6tm1c(EUCOMM)Wtsi Speer6-ps1Tg(Alb-cre)21Mgn
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Abcc6tm1c(EUCOMM)Wtsi mutation (1 available); any Abcc6 mutation (45 available)
E2f1Tg(Wnt1-cre)2Sor mutation (2 available); any E2f1 mutation (5 available)
Speer6-ps1Tg(Alb-cre)21Mgn mutation (5 available); any Speer6-ps1 mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism

integument
• 5 out of 13 mice exhibit calcification of the fibrous capsule surrounding the muzzle vibrissae occurs at 20 weeks of age

growth/size/body

craniofacial




Genotype
MGI:5662241
cn6
Allelic
Composition
Ggcxtm1Sino/Ggcx+
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
Genetic
Background
B6.Cg-Ggcxtm1Sino Speer6-ps1Tg(Alb-cre)21Mgn
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ggcxtm1Sino mutation (1 available); any Ggcx mutation (23 available)
Speer6-ps1Tg(Alb-cre)21Mgn mutation (5 available); any Speer6-ps1 mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
N
• none of the control heterozygotes died within the 100 days of the observation period




Genotype
MGI:5662240
cn7
Allelic
Composition
Ggcxtm1Sino/Ggcxtm1Sino
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
Genetic
Background
B6.Cg-Ggcxtm1Sino Speer6-ps1Tg(Alb-cre)21Mgn
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ggcxtm1Sino mutation (1 available); any Ggcx mutation (23 available)
Speer6-ps1Tg(Alb-cre)21Mgn mutation (5 available); any Speer6-ps1 mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice are born alive and survive for at least several weeks but die of fatal bleeding as a result of bleeding diathesis, injury and pregnancy
• when kept separately without mating, female mice survive significantly longer than male mice
• male mice begin to die from day 27 after birth, and all males die within 80 days after birth
• female mice begin to die from day 39 after birth and 7 out of 11 (63.6%) survive longer than 100 days, unless they become pregnant
• pregnancy causes fatal vaginal and uterine bleeding

cardiovascular system
• at 9 weeks of age, massive subcutaneous bleeding is noted even before death
• dissection of pregnant female mice just after death revealed uterine as well as vaginal bleeding

hematopoietic system
• mice appear to die of anemia secondary to bleeding

homeostasis/metabolism
• activities of vitamin K-dependent coagulation factors II and IX are significantly decreased relative to wild-type controls
• mice exhibit a bleeding diathesis and continue to bleed for >30 minutes after tail incision
• however, the platelet count is not significantly altered, suggesting that increased bleeding time is due to defective secondary coagulation

reproductive system
• dissection of pregnant female mice just after death revealed uterine as well as vaginal bleeding




Genotype
MGI:5538628
cn8
Allelic
Composition
Hmgcltm2Gam/Hmgcltm2Gam
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
Genetic
Background
B6.Cg-Hmgcltm2Gam Speer6-ps1Tg(Alb-cre)21Mgn
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hmgcltm2Gam mutation (0 available); any Hmgcl mutation (2 available)
Speer6-ps1Tg(Alb-cre)21Mgn mutation (5 available); any Speer6-ps1 mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

The leucine metabolite 2-ketoisocaproate induces liver steatosis in Hmgcltm2Gam/Hmgcltm2Gam Speer6-ps1Tg(Alb-cre)21Mgn/0 mice

mortality/aging
• all mice die between 3 and 5 weeks following spontaneous episodes, or crises, of progressive lethargy, hypoglycemia and hyperammonia
• however, mice fed a low protein diet plus 10% glucose in drinking water exhibit diminished occurrence of crises

homeostasis/metabolism
N
• mice exhibit normal peroxisome-related metabolites
• elevated levels of leucine-related metabolites in stressed mice (following injection of KIC or during spontaneous crises)
• increased plasma acylcarnities in stressed mice
• before death
• in mice treated with the leucine metabolite 2-ketoisocaproate (KIC)
• however, hyperammonemia is improved by carglumate treatment
• before death
• in mice treated with the leucine metabolite 2-ketoisocaproate (KIC)
• reduced gluconeogenesis in hepatocytes

liver/biliary system
• undetectable ketogenesis from octanoate in hepatocytes
• reduced gluconeogenesis in hepatocytes

behavior/neurological
• progressive 1 to 4 hours before death

cellular
• dilated in hepatocytes




Genotype
MGI:4439271
cn9
Allelic
Composition
Hs2st1tm1.1Je/Hs2st1tm1.1Je
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
Genetic
Background
B6.Cg-Hs2st1tm1.1Je Speer6-ps1Tg(Alb-cre)21Mgn
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hs2st1tm1.1Je mutation (1 available); any Hs2st1 mutation (9 available)
Speer6-ps1Tg(Alb-cre)21Mgn mutation (5 available); any Speer6-ps1 mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• mice exhibit slower plasma clearance of triglycerides and VLDL compared with wild-type mice
• however, plasma cholesterol levels are normal

liver/biliary system
• hepatocytes exhibit decreased VLDL binding, uptake, and degradation compared with wild-type cells




Genotype
MGI:5897809
cn10
Allelic
Composition
Mob1atm1.1Asuz/Mob1atm1.1Asuz
Mob1bGt(CC0690)Wtsi/Mob1bGt(CC0690)Wtsi
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
Genetic
Background
B6.Cg-Mob1bGt(CC0690)Wtsi Mob1atm1.1Asuz Speer6-ps1Tg(Alb-cre)21Mgn
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Mob1atm1.1Asuz mutation (0 available); any Mob1a mutation (8 available)
Mob1bGt(CC0690)Wtsi mutation (0 available); any Mob1b mutation (3 available)
Speer6-ps1Tg(Alb-cre)21Mgn mutation (5 available); any Speer6-ps1 mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• all mice are dead by 60 weeks
• the first mice die at P14 and more than half of mice die by P21

liver/biliary system
N
• mice exhibit normal liver structure at P0
• 3 times in controls
• at P7, mice exhibit increased immature cholangiocyte-like and oval cells that becomes massive at P10 especially in periductal and intraductal locations
• mild hepatocholangiocellular hyperplasia at P21
• 5 times greater than in control mice at P14
• massive
• combined hepatocellular and cholangiocarcinomas, increased hepatocellular carcinoma, liver adenoma incidence or cholangiocarcinoma in 8 of 10 mice surviving beyond P21 by age 15 weeks
• combined hepatocellular and cholangiocarcinomas in 13 of 22 mice at week 60
• with lung metastasis after 40 weeks of age
• intrahepatic cholangiocellular carcinoma in 8 of 10 mice surviving beyond P21 by age 15 weeks
• in 2 of 22 mice at week 60
• in mice surviving beyond P21 by age 15 weeks
• in 4 of 22 mice at week 60
• in mice surviving beyond P21 by age 15 weeks
• cholangiocytes proliferation is increased 4 times compared with controls
• however, there is no increase in apoptosis

neoplasm
• combined hepatocellular and cholangiocarcinomas, increased hepatocellular carcinoma, liver adenoma incidence or cholangiocarcinoma in 8 of 10 mice surviving beyond P21 by age 15 weeks
• combined hepatocellular and cholangiocarcinomas in 13 of 22 mice at week 60
• with lung metastasis after 40 weeks of age
• intrahepatic cholangiocellular carcinoma in 8 of 10 mice surviving beyond P21 by age 15 weeks
• in 2 of 22 mice at week 60
• in mice surviving beyond P21 by age 15 weeks
• in 4 of 22 mice at week 60
• in mice surviving beyond P21 by age 15 weeks

homeostasis/metabolism

integument
• due to enlarged liver

cellular
• 3 times in controls

endocrine/exocrine glands
• at P7, mice exhibit increased immature cholangiocyte-like and oval cells that becomes massive at P10 especially in periductal and intraductal locations
• mild hepatocholangiocellular hyperplasia at P21




Genotype
MGI:3697677
cn11
Allelic
Composition
Scarb1tm1Thh/Scarb1tm1Thh
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
Genetic
Background
B6.Cg-Scarb1tm1Thh Speer6-ps1Tg(Alb-cre)21Mgn
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Scarb1tm1Thh mutation (0 available); any Scarb1 mutation (7 available)
Speer6-ps1Tg(Alb-cre)21Mgn mutation (5 available); any Speer6-ps1 mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• elevation in plasma total cholesterol that is associated with more than 3-fold increase in free cholesterol
• high increase in plasma free cholesterol/plasma total cholesterol ratio
• develop severe hypercholesterolemia on an atherogenic diet due to an accumulation of free cholesterol-rich, VLDL-sized particles
• hepatic content of free and esterified cholesterol is normal
• marked elevation of HDL cholesterol with abnormally large HDL particles
• on an atherogenic diet, IL-6 plasma levels are 6.6-fold greater than in wild-type

cardiovascular system
• atherosclerosis is enhanced 32-fold compared to controls, when fed an atherogenic (high-fat, high-cholesterol, and cholic acid-containing) diet

immune system
• on an atherogenic diet, IL-6 plasma levels are 6.6-fold greater than in wild-type




Genotype
MGI:4867849
cn12
Allelic
Composition
Ahrb-1/Ahrb-1
Aiptm2.1Bra/Aiptm2.1Bra
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
Genetic
Background
B6.Cg-Speer6-ps1Tg(Alb-cre)21Mgn Aiptm2.1Bra
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ahrb-1 mutation (13 available); any Ahr mutation (76 available)
Aiptm2.1Bra mutation (0 available); any Aip mutation (9 available)
Speer6-ps1Tg(Alb-cre)21Mgn mutation (5 available); any Speer6-ps1 mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Ahrb-1/Ahrb-1 Aiptm2.1Bra/Aiptm2.1Bra Speer6-ps1Tg(Alb-cre)21Mgn/0 mice are resistant to dioxin-induced hepatic damage

homeostasis/metabolism
• doxin-treated mice do not exhibit an increase in serum alanine transaminase unlike similarly treated Aiptm2.1Bra homozygotes
• doxin-treated mice do not exhibit an increase in serum alanine transferase and are resistant to induced hepatic damage unlike similarly treated Aiptm2.1Bra homozygotes
• however, doxin-treated mice exhibit increased liver and thymus weight similar to wild-type mice

cardiovascular system
• in 1 of 8 mice

growth/size/body
• at 8 weeks

cellular
• in 1 of 8 mice




Genotype
MGI:5317915
cn13
Allelic
Composition
Naa40tm1Qwzh/Naa40tm1Qwzh
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
Genetic
Background
B6.Cg-Speer6-ps1Tg(Alb-cre)21Mgn Naa40tm1Qwzh
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Naa40tm1Qwzh mutation (0 available); any Naa40 mutation (16 available)
Speer6-ps1Tg(Alb-cre)21Mgn mutation (5 available); any Speer6-ps1 mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• at 22 weeks, but not 9 weeks, in male mice when normalized to body weight
• at 22 weeks, but not 9 weeks, in male mice when normalized to body weight
• during the dark cycle in male mice at 22 weeks
• slight in male mice, but not female mice
• hepatocytes exhibit decreased relative lipid synthesis compared with control cells
• fatty acid oxidation in the liver of male mice is increased compared to in control mice
• at 9 weeks, but not 31 weeks, in male mice
• at 31 weeks in male mice
• at 31 weeks in male mice

liver/biliary system
• at 31 weeks in male mice
• at 31 weeks in male mice
• induced by age or palmitic acid
• however, mice exhibit normal susceptibility to high fat diet-induced steatosis

adipose tissue
• at 6, 9 and 20 weeks

growth/size/body
• lean mass and content at 20 weeks in male mice, but not female mice
• slight in male mice, but not female mice

behavior/neurological
• slight in female and male mice fed standard chow
• in male mice fed a high fat diet

cellular
• fatty acid oxidation in the liver of male mice is increased compared to in control mice




Genotype
MGI:3773310
cn14
Allelic
Composition
Scd1tm2Ntam/Scd1tm2Ntam
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
Genetic
Background
B6.Cg-Speer6-ps1Tg(Alb-cre)21Mgn Scd1tm2Ntam
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Scd1tm2Ntam mutation (0 available); any Scd1 mutation (11 available)
Speer6-ps1Tg(Alb-cre)21Mgn mutation (5 available); any Speer6-ps1 mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
growth/size/body
• resistant to high carbohydrate and high-sucrose very low-fat, but not high fat, diet-induced obesity

adipose tissue
• reduced by 51% in mice on a high-sucrose very low-fat diet compared to diet matched controls
• on a high carbohydrate diet weights of the gonadal, retroperitioneal, and inguinal fat pads are reduced by about 49% - 59% compared to controls lacking the cre transgene
• reduced weight on a high carbohydrate diet compared to diet matched controls
• reduced weight on a high carbohydrate diet compared to diet matched controls
• reduced weight on a high carbohydrate diet compared to diet matched controls

homeostasis/metabolism
N
• unlike global null mice, no difference is seen in plasma glucose and insulin levels, glucose clearance or insulin sensitivity between liver knockout mice and controls on a high carbohydrate diet
• resistant to high carbohydrate and high-sucrose very low-fat, but not high fat, diet-induced obesity
• reduced in mice on a high-sucrose very low-fat diet compared to diet matched controls
• but not in mice on high carbohydrate, high fat, or chow diet
• supplementing the high-sucrose very low-fat diet with oleate prevents the decrease in plasma glucose levels
• impaired production of glucose from pyruvate in mice fed a high-sucrose very low-fat diet
• reduced in the liver in mice on a high-sucrose very low-fat diet compared to diet matched controls
• supplementing the diet with oleate prevents the decrease in hepatic glycogen levels
• 85% decrease in hepatic lipogenesis in mice on a high carbohydrate diet
• however, cholesterol synthesis is unaffected
• develops in mice on a high-sucrose very low-fat diet, probably due to increases in HDL and LDL cholesterol
• in mice on a high carbohydrate diet compared to diet-matched controls
• however, levels are similar to controls in mice on a chow or high fat diet
• significant reduction in mice on a high carbohydrate or a high-sucrose very low-fat diet compared to diet-matched controls
• on a high carbohydrate or diet high-sucrose very low-fat diet, liver triglyceride levels are reduced by 69% or 49%, respectively, compared to controls
• fasted mice refed a fat free high carbohydrate diet have lower liver levels of SCD1 products including palmitoleate and oleate
• supplementing the diet with triolein reduces the decrease in liver triglyceride levels

liver/biliary system
• on a high carbohydrate or diet high-sucrose very low-fat diet, liver triglyceride levels are reduced by 69% or 49%, respectively, compared to controls
• fasted mice refed a fat free high carbohydrate diet have lower liver levels of SCD1 products including palmitoleate and oleate
• supplementing the diet with triolein reduces the decrease in liver triglyceride levels
• resistant to high carbohydrate and high-sucrose very low-fat, but not high fat, diet-induced fatty liver development
• block in carbohydrate-induce hepatic lipogenesis
• a high-sucrose very low-fat diet fails to increase the rate of triglyceride secretion, unlike in controls

behavior/neurological
N
• unlike global null mice, no difference in food intake is seen in mice on a chow diet




Genotype
MGI:3629066
cn15
Allelic
Composition
Abcb7tm1Mdf/Y
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
Genetic
Background
either: B6.Cg-Speer6-ps1Tg(Alb-cre)21Mgn Abcb7tm1Mdf or (involves: 129S4/SvJae * 129S6/SvEvTac * C57BL/6 * DBA)
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Abcb7tm1Mdf mutation (1 available); any Abcb7 mutation (6 available)
Speer6-ps1Tg(Alb-cre)21Mgn mutation (5 available); any Speer6-ps1 mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
liver/biliary system
• mild hepatic architectural disarray and hepatocellular multinucleation are seen
• many cytosolic lipid droplets and pale swollen mitochondria are seen suggesting metabolic or mitochondrial damage
• multinucleated hepatocytes are seen

homeostasis/metabolism
• 2-fold increase in serum levels of liver-derived transaminases indicative of liver damage
• 76% increase in total liver iron; however, serum iron and total iron binding capacity are similar to controls and no signs of mitochondrial iron overload are detected
• a small subset of hepatocytes particularly cells adjacent to a portal triad or central vein, contain abundant, coarsely granular cytosolic iron deposits
• 50% reduction in hepatic activity of xanthine oxidase; however no change in expression is detected
• about a 20% decrease in hepatic mitochondrial activity of succinate dehydrogenase when normalized to cytochrome C oxidase activity
• about a 90% and 60% decrease in cytosolic aconitate hydratase 1 (Aco1) activity and protein, respectivly, are seen in the liver




Genotype
MGI:5316849
cn16
Allelic
Composition
Cav1tm1Pesch/Cav1tm1Pesch
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
Genetic
Background
FVB.Cg-Cav1tm1Pesch Speer6-ps1Tg(Alb-cre)21Mgn
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cav1tm1Pesch mutation (0 available); any Cav1 mutation (22 available)
Speer6-ps1Tg(Alb-cre)21Mgn mutation (5 available); any Speer6-ps1 mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• small but significant reduction in fasted glucose levels
• following 3-mercaptopicolinic acid treatment

liver/biliary system
N
• fasting induced steatosis and glycerol induced glucose production are similar to wild-type mice




Genotype
MGI:5824005
cn17
Allelic
Composition
Stk3tm1Jav/Stk3tm1Jav
Stk4Gt(AJ0315)Wtsi/Stk4Gt(AJ0315)Wtsi
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
Genetic
Background
involves: 129 * 129P2/OlaHsd * C57BL/6 * DBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Speer6-ps1Tg(Alb-cre)21Mgn mutation (5 available); any Speer6-ps1 mutation (2 available)
Stk3tm1Jav mutation (0 available); any Stk3 mutation (12 available)
Stk4Gt(AJ0315)Wtsi mutation (0 available); any Stk4 mutation (19 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
liver/biliary system
• mice develop multiple spontaneous hepatocellular carcinomas

neoplasm
• mice develop multiple spontaneous hepatocellular carcinomas

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
hepatocellular carcinoma DOID:684 OMIM:114550
J:238319




Genotype
MGI:3621473
cn18
Allelic
Composition
Arnttm1Bra/Arnttm1Bra
Vhltm1Jae/Vhltm1Jae
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
Genetic
Background
involves: 129 * BALB/c * C57BL/6 * DBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Arnttm1Bra mutation (0 available); any Arnt mutation (15 available)
Speer6-ps1Tg(Alb-cre)21Mgn mutation (5 available); any Speer6-ps1 mutation (2 available)
Vhltm1Jae mutation (2 available); any Vhl mutation (10 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
liver/biliary system
N
• livers appear histologically normal at 4 - 6 weeks of age




Genotype
MGI:3621471
cn19
Allelic
Composition
Hif1atm3Rsjo/Hif1atm3Rsjo
Vhltm1Jae/Vhltm1Jae
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
Genetic
Background
involves: 129 * BALB/c * C57BL/6 * DBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hif1atm3Rsjo mutation (3 available); any Hif1a mutation (10 available)
Speer6-ps1Tg(Alb-cre)21Mgn mutation (5 available); any Speer6-ps1 mutation (2 available)
Vhltm1Jae mutation (2 available); any Vhl mutation (10 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
liver/biliary system
• severe steatosis

cardiovascular system
• proliferation of endothelial cells in hepatic blood vessels
• hepatic vascular angiectasia

muscle
• hepatic vascular angiectasia

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
von Hippel-Lindau disease DOID:14175 OMIM:193300
J:97652




Genotype
MGI:4411991
cn20
Allelic
Composition
Stk3tm1Jav/Stk3tm1Jav
Stk4Gt(AJ0315)Wtsi/Stk4Gt(AJ0315)Wtsi
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
Genetic
Background
involves: 129 * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Speer6-ps1Tg(Alb-cre)21Mgn mutation (5 available); any Speer6-ps1 mutation (2 available)
Stk3tm1Jav mutation (0 available); any Stk3 mutation (12 available)
Stk4Gt(AJ0315)Wtsi mutation (0 available); any Stk4 mutation (19 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
liver/biliary system
• develop massively overgrown livers by 3 months of age (4 out of 4)
• develop hepatocellular carcinomas (HHCs) by 3 months of age (4 out of 4)

neoplasm
• develop hepatocellular carcinomas (HHCs) by 3 months of age (4 out of 4)




Genotype
MGI:5762654
cn21
Allelic
Composition
Gfertm1.1Crg/Gfertm1.1Crg
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
Genetic
Background
involves: 129 * C57BL/6 * DBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gfertm1.1Crg mutation (0 available); any Gfer mutation (16 available)
Speer6-ps1Tg(Alb-cre)21Mgn mutation (5 available); any Speer6-ps1 mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
liver/biliary system
• progressively coarsened and granular by 8 weeks
• after 6 months, mice develop nodular foci of high-grade dysplasia in the liver
• at 8 weeks of age
• focal hepatocyte necrosis at 4 weeks of age
• at 8 weeks of age
• modestly at 2 weeks of age
• however, levels are normal at 4 weeks of age
• at 2 and 4 weeks of age
• however, levels are normal at 8 weeks of age
• higher liver to body weight ratio at 4 to 6 weeks
• macro- and micro vesicular steatosis with hepatocyte swelling and minimal inflammation at 2 weeks of age
• reduced at 4 weeks of age
• pericellular fibrosis at 2 weeks of age
• periportal fibrosis at 4 weeks of age
• bridging fibrosis at 8 weeks of age
• milky white by 2 weeks of age
• however, livers regain normal color by 4 weeks
• at 1 year, most mice develop hepatocellular carcinomas with tumor cells that are pleomorphic and often steatotic with frequent mitotic figures and variably anaplastic nuclei
• prominent bile ductular proliferation at 4 weeks of age
• ductular proliferation at 8 weeks of age
• atypical ductular proliferation at 2 and 4 weeks of age
• cellular proliferation occurs in oval/biliary cells and parenchyma at 4 and 8 weeks of age
• at 2 weeks of age but decreasing progressively at 4 and 8 weeks of age
• scattered lobular mixed inflammation with focal hepatocyte necrosis and prominent bile ductular proliferation at 4 weeks of age
• increasing portal/perioral and lobular mixed inflammation
• increased proliferation at 4 and 8 weeks of age

homeostasis/metabolism
• at 8 weeks of age
• modestly at 2 weeks of age
• however, levels are normal at 4 weeks of age
• at 2 and 4 weeks of age
• however, levels are normal at 8 weeks of age

growth/size/body
• at 4 and 6 weeks
• however, body weight is normal at 1, 2 and 8 weeks

cellular
• dilated in hepatocytes with robust lipid deposition at 2 weeks of age; persistent to a lesser magnitude at 8 weeks
• swollen, abnormally shaped and with increased spacing or loss of cristae in hepatocyte mitochondria at 2 weeks of age; persistent to a lesser magnitude at 8 weeks
• increased spacing or loss of cristae in hepatocyte mitochondria at 2 weeks of age
• in hepatocyte mitochondria at 2 weeks of age
• in hepatocyte at 2 weeks of age
• in hepatocyte mitochondria at 2 weeks of age
• at 2 weeks of age but decreasing progressively at 4 and 8 weeks of age
• at 8 weeks of age
• focal hepatocyte necrosis at 4 weeks of age
• in hepatocyte mitochondria at 2 weeks of age
• however, respiration activity has recovered by 4 and 8 weeks of age

neoplasm
• at 1 year, most mice develop hepatocellular carcinomas with tumor cells that are pleomorphic and often steatotic with frequent mitotic figures and variably anaplastic nuclei

immune system
• scattered lobular mixed inflammation with focal hepatocyte necrosis and prominent bile ductular proliferation at 4 weeks of age
• increasing portal/perioral and lobular mixed inflammation




Genotype
MGI:3694896
cn22
Allelic
Composition
Ppargc1atm2Brsp/Ppargc1atm2Brsp
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
Genetic
Background
involves: 129 * C57BL/6 * DBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ppargc1atm2Brsp mutation (0 available); any Ppargc1a mutation (9 available)
Speer6-ps1Tg(Alb-cre)21Mgn mutation (5 available); any Speer6-ps1 mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cellular
• fasting-mediated induction of aminolevulinic acid synthase is decreased in mutants compared to wild-type

homeostasis/metabolism
• injection of lead chloride into fasted mice does not alter serum gamma-aminolevulinic acid (ALA) or porphobilinogen (PBG) in contrast to increased levels observed in wild-type




Genotype
MGI:5529807
cn23
Allelic
Composition
Ccn1tm3.1Lfl/Ccn1tm3.1Lfl
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
Genetic
Background
involves: 129 * C57BL/6 * DBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ccn1tm3.1Lfl mutation (0 available); any Ccn1 mutation (1 available)
Speer6-ps1Tg(Alb-cre)21Mgn mutation (5 available); any Speer6-ps1 mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
liver/biliary system
N
• mice exhibit normal liver morphology and outcome after partial hepatectomy
• CCl4-treated mice exhibit prominent central-to-central bridging fibrosis and a 4-fold increase more fibrotic area of collagen deposition in hydroxyproline accumulation compared with control mice
• 3 weeks following bile duct ligation, mice exhibit a 3-fold increase in fibrotic area compared with wild-type mice

homeostasis/metabolism
• CCl4-treated mice exhibit prominent central-to-central bridging fibrosis, a 4-fold increase more fibrotic area of collagen deposition, 3-fold increase in hydroxyproline accumulation and fewer senescence cells around the central vein compared with control mice
• 3 weeks following bile duct ligation, mice exhibit a 3-fold increase in fibrotic area and hydroxyproline content and fewer senescent cells compared with wild-type mice
• however, CCl4-treated mice exhibit normal level of liver damage (serum alanine aminotransferase, cell proliferation and cell apoptosis) and myofibroblast apoptosis

cellular
• fewer senescence cells surrounding the hepatic central veins in CCl4-treated mice




Genotype
MGI:4459910
cn24
Allelic
Composition
Hif1antm1.1Rsjo/Hif1antm1.1Rsjo
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
Genetic
Background
involves: 129 * C57BL/6 * DBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hif1antm1.1Rsjo mutation (0 available); any Hif1an mutation (9 available)
Speer6-ps1Tg(Alb-cre)21Mgn mutation (5 available); any Speer6-ps1 mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
normal phenotype




Genotype
MGI:6106900
cn25
Allelic
Composition
Nus1tm1.1Qrm/Nus1tm1.1Qrm
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
Genetic
Background
involves: 129 * C57BL/6 * DBA * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Nus1tm1.1Qrm mutation (0 available); any Nus1 mutation (4 available)
Speer6-ps1Tg(Alb-cre)21Mgn mutation (5 available); any Speer6-ps1 mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• induction of hepatic lipogenesis when fed Western diet
• both total and free when fed Western diet
• both total and free when fed Western diet
• when fed Western diet
• when fed Western diet

liver/biliary system
• both total and free when fed Western diet
• when fed Western diet
• when fed Western diet




Genotype
MGI:5318109
cn26
Allelic
Composition
Cdk1tm2.1Kald/Cdk1tm2.1Kald
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
Genetic
Background
involves: 129 * C57BL/6 * DBA * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdk1tm2.1Kald mutation (0 available); any Cdk1 mutation (16 available)
Speer6-ps1Tg(Alb-cre)21Mgn mutation (5 available); any Speer6-ps1 mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Livers of Cdk1tm2.1Kald/Cdk1tm2.1Kald Speer6-ps1Tg(Alb-cre)21Mgn/0 mice conatin fewer hepatocytes

liver/biliary system
• following partial hepatectomy, hepatocytes fail to enter cell division unlike control cells
• however, DNA replication is normal
• in untreated mice and following partial hepatectomy, hepatocytes exhibit increased nuclei diameter and decreased cell density compared with control cells
• in untreated mice and following partial hepatectomy

cellular
• in hepatocytes following partial hepatectomy
• following partial hepatectomy, hepatocytes fail to enter mitosis unlike control cells
• following partial hepatectomy, hepatocytes fail to enter cell division unlike control cells
• however, DNA replication is normal

neoplasm
• following tail-vein injection of activated Ras, mice fail to develop liver tumors unlike control mice

homeostasis/metabolism
• following partial hepatectomy, hepatocytes fail to enter cell division unlike control cells
• however, liver regeneration is achieved through cell growth




Genotype
MGI:6106901
cn27
Allelic
Composition
Nr1h3tm1Djm/Nr1h3tm1Djm
Nus1tm1.1Qrm/Nus1tm1.1Qrm
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
Genetic
Background
involves: 129 * C57BL/6 * DBA * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Nr1h3tm1Djm mutation (3 available); any Nr1h3 mutation (11 available)
Nus1tm1.1Qrm mutation (0 available); any Nus1 mutation (4 available)
Speer6-ps1Tg(Alb-cre)21Mgn mutation (5 available); any Speer6-ps1 mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
N
• when fed Western diet
• circulating triglyceride level
• liver triglyceride level
• circulating free fatty acid level
• liver free fatty acid level
• circulating cholesterol level both total and free
• both total and free when fed Western diet

liver/biliary system
• both total and free when fed Western diet




Genotype
MGI:5009547
cn28
Allelic
Composition
Ptpn11tm1Gsf/Ptpn11tm1Gsf
Stat3tm1Vpo/Stat3tm1Vpo
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
Genetic
Background
involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * C57BL/6 * DBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptpn11tm1Gsf mutation (0 available); any Ptpn11 mutation (12 available)
Speer6-ps1Tg(Alb-cre)21Mgn mutation (5 available); any Speer6-ps1 mutation (2 available)
Stat3tm1Vpo mutation (0 available); any Stat3 mutation (36 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• increase in serum ALT levels, however ALT levels are lower than in single conditional Ptpn11 mice
• mutants exhibit an increase in hepatocellular carcinoma development after diethylnitrosamine (DEN) injection compared to controls and single conditional Ptpn11 mutants, however tumor frequency and size are similar to that seen in single conditional Stat3 mutants

immune system
• infiltrate of inflammatory cells is seen in the portal triads of livers
• double mutants show less inflammation than seen in single conditional Ptpn11 mice, with reduced size of eosinophilic vacuoles of degeneration in the liver

liver/biliary system
• infiltrate of inflammatory cells is seen in the portal triads of livers
• double mutants show less inflammation than seen in single conditional Ptpn11 mice, with reduced size of eosinophilic vacuoles of degeneration in the liver

neoplasm
• mutants exhibit an increase in hepatocellular carcinoma development after diethylnitrosamine (DEN) injection compared to controls and single conditional Ptpn11 mutants, however tumor frequency and size are similar to that seen in single conditional Stat3 mutants




Genotype
MGI:5897813
cn29
Allelic
Composition
Ccn2tm1.1Alea/Ccn2tm1.1Alea
Mob1atm1.1Asuz/Mob1atm1.1Asuz
Mob1bGt(CC0690)Wtsi/Mob1bGt(CC0690)Wtsi
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
Genetic
Background
involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6 * DBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ccn2tm1.1Alea mutation (0 available); any Ccn2 mutation (15 available)
Mob1atm1.1Asuz mutation (0 available); any Mob1a mutation (8 available)
Mob1bGt(CC0690)Wtsi mutation (0 available); any Mob1b mutation (3 available)
Speer6-ps1Tg(Alb-cre)21Mgn mutation (5 available); any Speer6-ps1 mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
liver/biliary system
• increased immature cholangiocyte-like and oval cells as much as in Mob1atm1.1Asuz/Mob1atm1.1Asuz Mob1bGt(CC0690)Wtsi/Mob1bGt(CC0690)Wtsi Tg(Alb-cre)21Mgn mice
• as much as in Mob1atm1.1Asuz/Mob1atm1.1Asuz Mob1bGt(CC0690)Wtsi/Mob1bGt(CC0690)Wtsi Tg(Alb-cre)21Mgn mice
• as much as in Mob1atm1.1Asuz/Mob1atm1.1Asuz Mob1bGt(CC0690)Wtsi/Mob1bGt(CC0690)Wtsi Tg(Alb-cre)21Mgn mice

endocrine/exocrine glands
• increased immature cholangiocyte-like and oval cells as much as in Mob1atm1.1Asuz/Mob1atm1.1Asuz Mob1bGt(CC0690)Wtsi/Mob1bGt(CC0690)Wtsi Tg(Alb-cre)21Mgn mice




Genotype
MGI:3805348
cn30
Allelic
Composition
Irs1tm2Tka/Irs1tm2Tka
Irs2tm2Tka/Irs2tm2Tka
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * DBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Irs1tm2Tka mutation (0 available); any Irs1 mutation (28 available)
Irs2tm2Tka mutation (0 available); any Irs2 mutation (16 available)
Speer6-ps1Tg(Alb-cre)21Mgn mutation (5 available); any Speer6-ps1 mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• under fasting and refeeding conditions

immune system
• mice develop diabetes
• however, over-expression of a dominant negative Foxo1 by adenoviral transfection improves diabetes




Genotype
MGI:5428898
cn31
Allelic
Composition
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53+
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * DBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (6 available); any Kras mutation (35 available)
Speer6-ps1Tg(Alb-cre)21Mgn mutation (5 available); any Speer6-ps1 mutation (2 available)
Trp53tm1Brn mutation (13 available); any Trp53 mutation (150 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
liver/biliary system
• mutants develop intrahepatic cholangiocarcinoma as early as 32 weeks of age
• intrahepatic cholangiocarcinoma recapitulates the histologic and molecular features of multistage progression of human intrahepatic cholangiocarcinoma
• intrahepatic cholangiocarcinoma is associated with intraductal papillary neoplasms of the bile ducts and Von Meyenburg complexes, or biliary hamartomas
• intrahepatic cholangiocarcinoma is characterized by elevated levels of autophagy
• different grades of differentiation are seen in the same tumor

mortality/aging
• mean survival is 52 weeks of age

neoplasm
• mutants develop intrahepatic cholangiocarcinoma as early as 32 weeks of age
• intrahepatic cholangiocarcinoma recapitulates the histologic and molecular features of multistage progression of human intrahepatic cholangiocarcinoma
• intrahepatic cholangiocarcinoma is associated with intraductal papillary neoplasms of the bile ducts and Von Meyenburg complexes, or biliary hamartomas
• intrahepatic cholangiocarcinoma is characterized by elevated levels of autophagy
• different grades of differentiation are seen in the same tumor
• tumors are highly metastatic, with tumors showing invasion into adjacent organs such as the diaphragm, bowel, pancreas and stomach or distant metastasis to the lymph nodes, spleen, lungs, or peritoneal cavity
• intrahepatic cholangiocarcinoma is associated with biliary hamartomas

cardiovascular system
• hepatic lesions frequently show hemorrhage into the peritoneal cavity and exhibit evidence of tumor necrosis

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
intrahepatic cholangiocarcinoma DOID:4928 J:184949




Genotype
MGI:5618808
cn32
Allelic
Composition
Atp8b1tm1Nbf/Atp8b1tm1Nbf
Portm1Wolf/Portm1Wolf
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * DBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Atp8b1tm1Nbf mutation (2 available); any Atp8b1 mutation (2 available)
Portm1Wolf mutation (2 available); any Por mutation (52 available)
Speer6-ps1Tg(Alb-cre)21Mgn mutation (5 available); any Speer6-ps1 mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• mice fed a cholic acid-supplemented diet for 4 weeks starting at 4 weeks of age, exhibit a slight increase in bile duct proliferation

mortality/aging
• mice fed a 0.03% cholic acid-supplemented diet directly from weaning die within a week after the start of the diet
• however, mice fed a 0.03% cholic acid-supplemented diet starting at 4 weeks of age for 4 weeks survive

growth/size/body
• mice fail to gain weight and even lose weight after starting of 0.03% cholic acid-supplemented diet at 4 weeks of age

homeostasis/metabolism
• after 4 weeks of cholic acid-supplemented diet started at 4 weeks of age, mice exhibit enhanced plasma bilirubin levels
• after 4 weeks of cholic acid-supplemented diet started at 4 weeks of age, mice exhibit a mild elevation in plasma alanine transaminase levels
• after 4 weeks of cholic acid-supplemented diet started at 4 weeks of age, mice exhibit a mild elevation in plasma alkaline phosphatase levels
• after 4 weeks on a cholic acid-supplemented diet, plasma bile salts predominantly consist of about 90% taurocholate (TC) and about 7% tauro-beta-muricholate (TbetaMC) and a low concentration of about 0.4% of the secondary bile salt taurochenodeoxycholate (TDC) is seen compared to about 70% TC and 20% TbetaMC in single Atp8b1 homozygotes
• after 4 weeks on a cholic acid-supplemented diet, biliary bile salts predominantly consist of about 90% TC and about 9% TbetaMC compared to 55% TC and 40% TbetaMC in single Atp8b1 homozygotes
• after 4 weeks on a cholic acid-supplemented diet, bile salt hydrophobicity index of plasma is elevated but the hydrophobicity index of bile is unaltered, indicating that the plasma bile salt pool is more hydrophobic
• after 4 weeks of cholic acid-supplemented diet started at 4 weeks of age, mice exhibit a strong elevation in plasma bile salt levels

liver/biliary system
• mice fed a cholic acid-supplemented diet for 4 weeks starting at 4 weeks of age, exhibit a slight increase in bile duct proliferation
• liver weights are increased in mice fed a cholic acid-supplemented diet for 4 weeks starting at 4 weeks of age
• mice fed a cholic acid-supplemented diet for 4 weeks starting at 4 weeks of age do not exhibit fibrosis in the liver
• after 4 weeks of cholic acid-supplemented diet started at 4 weeks of age, bile flow is strongly (about 3-fold) reduced
• mice, however show normal bile salt output when fed a cholic acid-supplemented diet for 4 weeks starting at 4 weeks of age
• mice fed a cholic acid-supplemented diet for 4 weeks starting at 4 weeks of age develop a severe cholestatic phenotype with mild liver damage

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
intrahepatic cholestasis DOID:1852 J:215915




Genotype
MGI:6256732
cn33
Allelic
Composition
Krastm4Tyj/Kras+
Ptentm2Mak/Pten+
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * DBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (6 available); any Kras mutation (35 available)
Ptentm2Mak mutation (4 available); any Pten mutation (39 available)
Speer6-ps1Tg(Alb-cre)21Mgn mutation (5 available); any Speer6-ps1 mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• some lesions are diagnosed as intrahepatic cholangiocarcinoma by the appearance of adenocarcinoma showing tubular and/or papillary structures with a fibrous stroma; these tumor cells show loss of Pten expression
• mice develop liver tumors at 6 months of age, showing obvious symptoms after 7 months with abdominal distension due to multiple tumors at later stages
• mice develop liver tumors with both hepatocyte and cholangiocyte differentiation
• majority of large nodules are hepatocellular dysplasia, a precursor lesion of hepatocellular carcinoma

liver/biliary system
• some lesions are diagnosed as intrahepatic cholangiocarcinoma by the appearance of adenocarcinoma showing tubular and/or papillary structures with a fibrous stroma; these tumor cells show loss of Pten expression
• mice develop liver tumors at 6 months of age, showing obvious symptoms after 7 months with abdominal distension due to multiple tumors at later stages
• mice develop liver tumors with both hepatocyte and cholangiocyte differentiation
• majority of large nodules are hepatocellular dysplasia, a precursor lesion of hepatocellular carcinoma




Genotype
MGI:6256730
cn34
Allelic
Composition
Krastm4Tyj/Kras+
Ptentm2Mak/Ptentm2Mak
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * DBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (6 available); any Kras mutation (35 available)
Ptentm2Mak mutation (4 available); any Pten mutation (39 available)
Speer6-ps1Tg(Alb-cre)21Mgn mutation (5 available); any Speer6-ps1 mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• median survival is 46 days

growth/size/body
• seen in 5 month old mice
• all mice start to show abdominal distension at about 5 weeks of age, frequently accompanied by jaundice and weight loss
• distension is due to hepatic enlargement and/or hemorrhagic ascites

neoplasm
• tumors primarily show glandular morphology that resembles well-differentiated human cholangiocarcinoma and marker analysis indicates that tumors are intrahepatic cholangiocarcinoma
• in some cases, regions of moderately differentiated tumor with a cribriform appearance are seen
• no metastasis or invasion to other organs is seen
• tumors are frequently surrounded by dense fibrous stroma, indicating accumulation of fibrillar collagens
• stellate cells are activated and acquire a myofibroblast-like phenotype
• tumor cells show mucin production, a characteristic of epithelial cells in the bile duct
• multiple solid tumors with various sizes are seen throughout the liver
• invasive tumors are apparent after 7 weeks of age, with abundant desmoplastic stroma or desmoplasia

endocrine/exocrine glands
• various degrees of hyperplasia are seen in the bile ducts, characterized by increase in number and size and change in morphology, at 4 weeks of age
• at 5 weeks, a part of the hyperplastic ductal lesions at the hilum become enlarged and show a pattern of papillary growth

homeostasis/metabolism

liver/biliary system
• various degrees of hyperplasia are seen in the bile ducts, characterized by increase in number and size and change in morphology, at 4 weeks of age
• at 5 weeks, a part of the hyperplastic ductal lesions at the hilum become enlarged and show a pattern of papillary growth
• tumors primarily show glandular morphology that resembles well-differentiated human cholangiocarcinoma and marker analysis indicates that tumors are intrahepatic cholangiocarcinoma
• in some cases, regions of moderately differentiated tumor with a cribriform appearance are seen
• no metastasis or invasion to other organs is seen
• tumors are frequently surrounded by dense fibrous stroma, indicating accumulation of fibrillar collagens
• stellate cells are activated and acquire a myofibroblast-like phenotype
• tumor cells show mucin production, a characteristic of epithelial cells in the bile duct
• invasive tumors are apparent after 7 weeks of age, with abundant desmoplastic stroma or desmoplasia
• multiple solid tumors with various sizes are seen throughout the liver
• seen in 5 month old mice

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
intrahepatic cholangiocarcinoma DOID:4928 J:254370




Genotype
MGI:5428907
cn35
Allelic
Composition
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm1Brn
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * DBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (6 available); any Kras mutation (35 available)
Speer6-ps1Tg(Alb-cre)21Mgn mutation (5 available); any Speer6-ps1 mutation (2 available)
Trp53tm1Brn mutation (13 available); any Trp53 mutation (150 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
liver/biliary system
• mutants develop intrahepatic cholangiocarcinoma as early as 9 weeks of age
• intrahepatic cholangiocarcinoma is associated with intraductal papillary neoplasms of the bile ducts and Von Meyenburg complexes, or biliary hamartomas
• intrahepatic cholangiocarcinoma is characterized by elevated levels of autophagy
• different grades of differentiation are seen in the same tumor

mortality/aging
• mean survival is 19 weeks of age

neoplasm
• mutants develop intrahepatic cholangiocarcinoma as early as 9 weeks of age
• intrahepatic cholangiocarcinoma is associated with intraductal papillary neoplasms of the bile ducts and Von Meyenburg complexes, or biliary hamartomas
• intrahepatic cholangiocarcinoma is characterized by elevated levels of autophagy
• different grades of differentiation are seen in the same tumor
• tumors are highly metastatic, with 75% of mutants having tumors showing invasion into adjacent organs such as the diaphragm, bowel, pancreas and stomach or distant metastasis to the lymph nodes, spleen, lungs, or peritoneal cavity
• intrahepatic cholangiocarcinoma is associated with biliary hamartomas

cardiovascular system
• hepatic lesions frequently show hemorrhage into the peritoneal cavity and exhibit evidence of tumor necrosis

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
intrahepatic cholangiocarcinoma DOID:4928 J:184949




Genotype
MGI:4838529
cn36
Allelic
Composition
Akt2tm1.1Mbb/Akt2tm1.1Mbb
Ptentm1Hwu/Ptentm1Hwu
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * DBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Akt2tm1.1Mbb mutation (2 available); any Akt2 mutation (25 available)
Ptentm1Hwu mutation (3 available); any Pten mutation (39 available)
Speer6-ps1Tg(Alb-cre)21Mgn mutation (5 available); any Speer6-ps1 mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• about 25-30% increase in fasting glucose levels at 1 month of age
• glucose intolerance

liver/biliary system
N
• the liver phenotype observed in single Pten mutants is significantly reduced, with liver weights, triglyceride levels in the liver and fatty liver almost similar to controls
• progenitor cell accumulation in the periductal region of livers occurs later than in single conditional Pten homozygotes, when injury conditions are already present
• mice do not show development of steatosis compared to single conditional Pten homozygotes

neoplasm
• mice exhibit a 6-month delay in liver tumor onset compared to conditional Pten homozygotes
• no mice develop liver tumors between 9 and 12 months of age and 25% of mice older than 12 months develop liver nodules
• however, treatment of 3 month old mice with 3,5-dietoxycarbonyl-1,4 dihydrocollidine (DDC) to induce liver injury leads to massive expansion of hepatic progenitors and development of premalignant lesions




Genotype
MGI:4819844
cn37
Allelic
Composition
Krastm4Tyj/Krastm4Tyj
Yap1tm1.1Dupa/Yap1tm1.1Dupa
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * DBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (6 available); any Kras mutation (35 available)
Speer6-ps1Tg(Alb-cre)21Mgn mutation (5 available); any Speer6-ps1 mutation (2 available)
Yap1tm1.1Dupa mutation (2 available); any Yap1 mutation (17 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
liver/biliary system

neoplasm




Genotype
MGI:3041261
cn38
Allelic
Composition
Mettm1Sst/Mettm1Sst
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Mettm1Sst mutation (1 available); any Met mutation (4 available)
Speer6-ps1Tg(Alb-cre)21Mgn mutation (5 available); any Speer6-ps1 mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mutants are more vulnerable to hepatectomy surgery and most are either moribund or die by 48 hours after surgery

liver/biliary system
• mutants develop hemorrhagic liver destruction within the first few hours in response to apoptotic stimuli induced by Fas (Tnfrsf6) antibody compared to only minor liver damage in controls
• primary hepatocytes show reduced phagocytic activity towards bacteria (E.coli) than control cells
• hepatocytes exhibit increased sensitivity to Fas (Tnfrsf6)-induced apoptosis
• the ability of mutant livers to clear necrotic tissue and to repopulate the injured (by CCl4 exposure) area by regenerating hepatocytes is impaired
• associated with a persistent inflammatory reaction, overproduction of osteopontin, early and prominent dystrophic calcification, and impaired hepatocyte scattering/migration into diseased areas
• 80% of mutants die of acute liver failure in response to apoptotic stimuli induced by Fas (Tnfrsf6) antibody while controls survive

cardiovascular system
• mutants develop hemorrhagic liver destruction within the first few hours in response to apoptotic stimuli induced by Fas (Tnfrsf6) antibody compared to only minor liver damage in controls

homeostasis/metabolism
• mutants exhibit delayed healing after toxic liver injury induced by CCl4 exposure
• mutants are more vulnerable to hepatectomy surgery and most are either moribund or die by 48 hours after surgery
• hepatocytes fail to migrate in a standard wound healing assay

cellular
• hepatocytes exhibit increased sensitivity to Fas (Tnfrsf6)-induced apoptosis




Genotype
MGI:5702658
cn39
Allelic
Composition
Ptentm2Mak/Ptentm2Mak
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * C57BL/6J * DBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptentm2Mak mutation (4 available); any Pten mutation (39 available)
Speer6-ps1Tg(Alb-cre)21Mgn mutation (5 available); any Speer6-ps1 mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
liver/biliary system
• mild sinusoidal fibrogenic changes and accumulations of lobular inflammatory cells are seen by 40 weeks of age
• increase in hepatocyte proliferation at 10 weeks of age
• however, no differences in hepatocyte apoptosis are seen at 10 or 40 weeks of age
• triglyceride levels are increased in the liver at 10 weeks of age and are highly elevated at 40 weeks of age
• however, no differences in liver levels of free fatty acids, free cholesterol, or phospholipids are seen
• hepatocytes acquire expression of an adipocyte-specific marker
• Mallory bodies are frequently seen in hepatocytes by 40 weeks of age
• absolute numbers of total liver cells are almost normal at 10 weeks of age but increased by 1.5-fold at 40 weeks
• liver is larger in 10 week old mice and further enlarged at 40 weeks
• liver weight per body weight ratio is increased 2-fold at 10 weeks and 3-fold at 40 weeks
• cytoplasm of liver cells is weakly eosinophilic and contains numerous microvesicular vacuoles containing lipids at 10 weeks of age; vacuolar changes are seen mainly around the central vein
• steatotic changes are more prominent in male than female mice
• by 40 weeks of age, livers show fatty changes of increased severity throughout the hepatic lobule such that aged liver resembles adipocytes in fat tissues
• however, no fibrotic changes are seen in the liver
• livers are light-colored at 10 weeks of age and homogenously white in color at 40 weeks
• hepatocellular carcinomas are seen in 5 of 6 males and 3 of 6 females; the hepatocellular carcinomas develop within liver adenomas and contain many fewer cytoplasmic lipid droplets than the adenomas
• macroscopic hepatic tumors are present in 66% of male and 30% of female mice at 40-44 weeks of age; nodular lesions resemble liver adenomas and cells with large droplets in the cytoplasm are prominent in most adenomas

homeostasis/metabolism
• cholesterol ester levels are increased in the liver at 10 weeks of age and are highly elevated at 40 weeks of age
• glucose levels are lower in fasted mutants both before and after oral glucose administration
• serum insulin levels are reduced at 12 weeks of age
• serum levels are elevated at 40 weeks of age but not at 10 weeks of age
• serum levels are elevated at 40 weeks of age but not at 10 weeks of age
• serum levels are elevated at 40 weeks of age but not at 10 weeks of age
• intraperitoneal insulin injection reduces glucose levels by a greater amount than in wild-type mice indicating insulin hypersensitivity
• 16-carbon monosaturated fatty acids (C16:1) and C18:1 fatty acids are increased in livers of 10 week old mice and C16:0, C16:1, C18:0, C18:1, and C18:2 fatty acids are increased in livers of 40 week old mice
• triglyceride levels are increased in the liver at 10 weeks of age and are highly elevated at 40 weeks of age
• however, no differences in liver levels of free fatty acids, free cholesterol, or phospholipids are seen

neoplasm
• hepatocellular carcinomas are seen in 5 of 6 males and 3 of 6 females; the hepatocellular carcinomas develop within liver adenomas and contain many fewer cytoplasmic lipid droplets than the adenomas
• macroscopic hepatic tumors are present in 66% of male and 30% of female mice at 40-44 weeks of age; nodular lesions resemble liver adenomas and cells with large droplets in the cytoplasm are prominent in most adenomas
• 2 mutants with hepatocellular carcinoma show lung metastasis

cardiovascular system
• mild sinusoidal fibrogenic changes and accumulations of lobular inflammatory cells are seen by 40 weeks of age

cellular
• increase in hepatocyte proliferation at 10 weeks of age
• however, no differences in hepatocyte apoptosis are seen at 10 or 40 weeks of age
• cholesterol ester levels are increased in the liver at 10 weeks of age and are highly elevated at 40 weeks of age
• hepatic hydrogen peroxide levels in the liver are increased 7-fold, indicating increased production of reactive oxygen species




Genotype
MGI:5897815
cn40
Allelic
Composition
Mob1atm1.1Asuz/Mob1atm1.1Asuz
Mob1bGt(CC0690)Wtsi/Mob1bGt(CC0690)Wtsi
Yap1tm1c(KOMP)Mbp/Yap1tm1c(KOMP)Mbp
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * C57BL/6N * DBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Mob1atm1.1Asuz mutation (0 available); any Mob1a mutation (8 available)
Mob1bGt(CC0690)Wtsi mutation (0 available); any Mob1b mutation (3 available)
Speer6-ps1Tg(Alb-cre)21Mgn mutation (5 available); any Speer6-ps1 mutation (2 available)
Yap1tm1c(KOMP)Mbp mutation (0 available); any Yap1 mutation (17 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
liver/biliary system
• increased immature cholangiocyte-like and oval cells but far less than in Mob1atm1.1Asuz/Mob1atm1.1Asuz Mob1bGt(CC0690)Wtsi/Mob1bGt(CC0690)Wtsi Tg(Alb-cre)21Mgn mice
• much less than in Mob1atm1.1Asuz/Mob1atm1.1Asuz Mob1bGt(CC0690)Wtsi/Mob1bGt(CC0690)Wtsi Tg(Alb-cre)21Mgn mice
• much less than in Mob1atm1.1Asuz/Mob1atm1.1Asuz Mob1bGt(CC0690)Wtsi/Mob1bGt(CC0690)Wtsi Tg(Alb-cre)21Mgn mice

endocrine/exocrine glands
• increased immature cholangiocyte-like and oval cells but far less than in Mob1atm1.1Asuz/Mob1atm1.1Asuz Mob1bGt(CC0690)Wtsi/Mob1bGt(CC0690)Wtsi Tg(Alb-cre)21Mgn mice




Genotype
MGI:2177363
cn41
Allelic
Composition
Foxa2tm1Khk/Foxa2tm1Khk
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * CD-1 * DBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Foxa2tm1Khk mutation (1 available); any Foxa2 mutation (21 available)
Speer6-ps1Tg(Alb-cre)21Mgn mutation (5 available); any Speer6-ps1 mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
normal phenotype
• homozygous mice exhibit no discernable phenotype; mice are viable and fertile with normal liver metabolism and normal glucose homeostasis




Genotype
MGI:3620114
cn42
Allelic
Composition
Rr27tm2Msb/Rr27+
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * DBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Rr27tm2Msb mutation (1 available); any Rr27 mutation (5 available)
Speer6-ps1Tg(Alb-cre)21Mgn mutation (5 available); any Speer6-ps1 mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cellular
• paternal allele specific methylation is maintained
• maternal Igf2 allele expression is detected in the neonate liver
• paternal Igf2 allele expression is reduced




Genotype
MGI:3620636
cn43
Allelic
Composition
Keap1tm1Mym/Keap1tm2Mym
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * DBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Keap1tm1Mym mutation (1 available); any Keap1 mutation (18 available)
Keap1tm2Mym mutation (0 available); any Keap1 mutation (18 available)
Speer6-ps1Tg(Alb-cre)21Mgn mutation (5 available); any Speer6-ps1 mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• unlike most wild-type mice, mutant mice survive following intraperitoneal administration of 600-mg or 700-mg acetaminophen/kg body weight

homeostasis/metabolism
• unlike most wild-type mice, mutant mice survive following intraperitoneal administration of 600-mg or 700-mg acetaminophen/kg body weight
• much milder hepatic injury in livers of mutant mice following acetaminophen exposure




Genotype
MGI:3805350
cn44
Allelic
Composition
Irs1tm2Tka/Irs1tm2Tka
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * DBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Irs1tm2Tka mutation (0 available); any Irs1 mutation (28 available)
Speer6-ps1Tg(Alb-cre)21Mgn mutation (5 available); any Speer6-ps1 mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
N
• mice exhibit normal hepatic triglyceride content, serum aspartate aminotransferase and alanine aminotransferase indicating a lack of hepatic injury
• mice exhibit higher serum insulin levels 4 and 6 hours after the start of refeeding unlike wild-type mice
• mice exhibit insulin resistance under refeeding conditions
• however, mice do not exhibit insulin resistance under fasting conditions




Genotype
MGI:3806986
cn45
Allelic
Composition
Ptentm2Mak/Ptentm2Mak
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * DBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptentm2Mak mutation (4 available); any Pten mutation (39 available)
Speer6-ps1Tg(Alb-cre)21Mgn mutation (5 available); any Speer6-ps1 mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
liver/biliary system
• at 10 weeks of age
• by 40 weeks of age, livers contain Mallory bodies, ballooning hepatocytes and accumulation of lobular inflammatory cells
• at 10 and 40 weeks of age
• at 10 and 40 weeks of age
• at 10 weeks of age, the cytoplasm of hepatocytes contain lipid-filled micro- and macro-vesicular vacuoles unlike in wild-type mice
• at 40 weeks of age, micro- and macro-vesicular vacuoles coalesce to and displace the nucleus
• by 40 weeks of age, livers contain Mallory bodies
• beginning at 10 weeks of age, mice exhibit enlargement of the liver that progressed further by 40 weeks of age
• at 10 weeks of age
• at 40 weeks of age
• beginning at 10 weeks of age, mice exhibit a pale liver that is white by 40 weeks of age
• at 74 to 78 weeks of age, 83% of males and 50% of females exhibit hepatocellular carcinomas that develop within liver adenomas and contain fewer lipid droplets than the adenomas
• 2 of 6 mice exhibit metastasis of hepatocellular carcinomas to the lungs
• at 40 weeks of age, 66% of males and 30% of females exhibit liver adenomas that contain large lipid droplets
• the polyploid mononuclear hepatocyte population is enriched in the liver of 3 and 10 month old mutants
• highly polyploid hepatocytes are also present in hepatocellular tumors in the livers
• at 10 weeks of age, hepatocyte proliferation is increased while apoptosis rates are normal

neoplasm
• at 74 to 78 weeks of age, 83% of males and 50% of females exhibit hepatocellular carcinomas that develop within liver adenomas and contain fewer lipid droplets than the adenomas
• 2 of 6 mice exhibit metastasis of hepatocellular carcinomas to the lungs
• at 40 weeks of age, 66% of males and 30% of females exhibit liver adenomas that contain large lipid droplets

homeostasis/metabolism
• at 10 and 40 weeks of age
• at 10 and 40 weeks of age

immune system
• at 10 weeks of age

cellular
• at 10 weeks of age, hepatocyte proliferation is increased while apoptosis rates are normal

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
hepatocellular carcinoma DOID:684 OMIM:114550
J:138099




Genotype
MGI:3826674
cn46
Allelic
Composition
Cyb5atm1Wolf/Cyb5atm1Wolf
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * DBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cyb5atm1Wolf mutation (0 available); any Cyb5a mutation (4 available)
Speer6-ps1Tg(Alb-cre)21Mgn mutation (5 available); any Speer6-ps1 mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• early (0 to 60 minutes) concentrations of a drug mixture, which contains midazolam, phenacetin, metaprodol, chlorzoxazone and tolbutamide, administered intravenously are higher than in wild-type mice
• at 2 hours, concentrations of the drug mixture administered intravenously was lower than in wild-type mice
• mice exhibit faster drug clearance and AUC (except in the case of midazolam) compared to wild-type mice
• the half-lives of phenacetin, tolbutamide, chlorzozane and midazolam are longer than in wild-type mice
• metabolite production following administration of drugs intravenously is shifted to the right compared to in wild-type mice
• when the drug mixture is given orally, AUC, Cmax are higher and clearance is slower than in wild-type mice for midazolam, phenacetin and metoprolol
• AUC and Cmax for tolbutamide given orally are lower than in wild-type mice
• when tolbutamide is administered orally or intravenously on its own, AUC and Cmax are increased and clearance is decreased compared to in wild-type mice
• mice exhibit a 4-fold increase in bioavailability of orally administered midazolam compared to in wild-type mice
• mice exhibit a 50% decrease in bioavailability of tolbutamide when delivered in a mixture and a 100% increase in bioavailability when administered on its own compared to in wild-type mice

liver/biliary system
N
• liver morphology is normal




Genotype
MGI:4417849
cn47
Allelic
Composition
Acsl1tm1Rcol/Acsl1tm1Rcol
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * DBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Acsl1tm1Rcol mutation (1 available); any Acsl1 mutation (25 available)
Speer6-ps1Tg(Alb-cre)21Mgn mutation (5 available); any Speer6-ps1 mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
growth/size/body
N
• normal body weight and organ weights

adipose tissue
N
• normal adiposity

homeostasis/metabolism
N
• normal plasma levels of metabolites
• normal golucose tolerance tests and insulin tolerance tests
• liver acyl-CoA levels are 35% lower than controls on a normal diet and 25% lower than controls on a high fat diet




Genotype
MGI:4819841
cn48
Allelic
Composition
Yap1tm1.1Dupa/Yap1tm1.1Dupa
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * DBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Speer6-ps1Tg(Alb-cre)21Mgn mutation (5 available); any Speer6-ps1 mutation (2 available)
Yap1tm1.1Dupa mutation (2 available); any Yap1 mutation (17 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
liver/biliary system
• at 1 to 2 months
• after 30 weeks, mice lack bile ducts or bile duct-like structures unlike wild-type mice
• livers fail to form mature bile ducts unlike in wild-type mice
• at 1 to 2 months, the liver contains multiple areas of injured hepatocytes unlike in wild-type mice
• macrovesicular
• mice exhibit progressive liver fibrosis with early periportal fibrosis at 20 weeks unlike wild-type mice
• at 30 weeks, mice exhibit advanced fibrosis with cirrhosis unlike wild-type mice

homeostasis/metabolism

endocrine/exocrine glands
• after 30 weeks, mice lack bile ducts or bile duct-like structures unlike wild-type mice
• livers fail to form mature bile ducts unlike in wild-type mice

cellular
• at 1 to 2 months




Genotype
MGI:4819842
cn49
Allelic
Composition
Nf2tm2Gth/Nf2tm2Gth
Yap1tm1.1Dupa/Yap1tm1.1Dupa
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * DBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Nf2tm2Gth mutation (3 available); any Nf2 mutation (68 available)
Speer6-ps1Tg(Alb-cre)21Mgn mutation (5 available); any Speer6-ps1 mutation (2 available)
Yap1tm1.1Dupa mutation (2 available); any Yap1 mutation (17 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
liver/biliary system
N
• liver is as enlarge as in Nf2tm2Gth/Nf2tm2Gth Tg(Alb-cre)21Mgn mice
• bile over-proliferation observed in Nf2tm2Gth/Nf2tm2Gth Tg(Alb-cre)21Mgn mice is suppressed

neoplasm
N
• mice do not develop bile duct hamartomas or hepatocellular carcinoma unlike Nf2tm2Gth/Nf2tm2Gth Tg(Alb-cre)21Mgn mice




Genotype
MGI:4819843
cn50
Allelic
Composition
Nf2tm2Gth/Nf2tm2Gth
Yap1tm1.1Dupa/Yap1+
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * DBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Nf2tm2Gth mutation (3 available); any Nf2 mutation (68 available)
Speer6-ps1Tg(Alb-cre)21Mgn mutation (5 available); any Speer6-ps1 mutation (2 available)
Yap1tm1.1Dupa mutation (2 available); any Yap1 mutation (17 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
liver/biliary system
N
• mice do not exhibit bile duct proliferation
• slightly

neoplasm
N
• mice do not develop bile duct hamartomas or hepatocellular carcinoma




Genotype
MGI:4819845
cn51
Allelic
Composition
Nf2tm2Gth/Nf2tm2Gth
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * DBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Nf2tm2Gth mutation (3 available); any Nf2 mutation (68 available)
Speer6-ps1Tg(Alb-cre)21Mgn mutation (5 available); any Speer6-ps1 mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
liver/biliary system
• at E18.5, multiple tubular structures surround each portal vein unlike in wild-type mice
• mice exhibit widespread bile duct hamartomas that expand into the deep liver parenchyma unlike wild-type mice

neoplasm
• mice exhibit widespread bile duct hamartomas that expand into the deep liver parenchyma unlike wild-type mice

endocrine/exocrine glands




Genotype
MGI:5912277
cn52
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Smarcd1tm1.1Jddl/Smarcd1tm1.1Jddl
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * DBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (31 available); any Apoe mutation (96 available)
Smarcd1tm1.1Jddl mutation (0 available); any Smarcd1 mutation (11 available)
Speer6-ps1Tg(Alb-cre)21Mgn mutation (5 available); any Speer6-ps1 mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• area of atherosclerotic lesions is reduced by about 53% compared to mice homozygous null for Apoe alone

homeostasis/metabolism
• cholesterol levels are approximately 30% lower in Western diet fed mice compared to diet matched controls
• expression analysis indicates bile acid metabolism is reduced




Genotype
MGI:5009548
cn53
Allelic
Composition
Stat3tm1Vpo/Stat3tm1Vpo
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * DBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Speer6-ps1Tg(Alb-cre)21Mgn mutation (5 available); any Speer6-ps1 mutation (2 available)
Stat3tm1Vpo mutation (0 available); any Stat3 mutation (36 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• mutants exhibit an increase in hepatocellular carcinoma development (increase in tumor number and size) after diethylnitrosamine (DEN) injection compared to controls

neoplasm
• mutants exhibit an increase in hepatocellular carcinoma development (increase in tumor number and size) after diethylnitrosamine (DEN) injection compared to controls




Genotype
MGI:5897816
cn54
Allelic
Composition
Mob1atm1.1Asuz/Mob1atm1.1Asuz
Mob1bGt(CC0690)Wtsi/Mob1bGt(CC0690)Wtsi
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
Tgfbr2tm1Roes/Tgfbr2tm1Roes
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * DBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Mob1atm1.1Asuz mutation (0 available); any Mob1a mutation (8 available)
Mob1bGt(CC0690)Wtsi mutation (0 available); any Mob1b mutation (3 available)
Speer6-ps1Tg(Alb-cre)21Mgn mutation (5 available); any Speer6-ps1 mutation (2 available)
Tgfbr2tm1Roes mutation (2 available); any Tgfbr2 mutation (7 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
liver/biliary system
• increased immature cholangiocyte-like and oval cells but not as much as in Mob1atm1.1Asuz/Mob1atm1.1Asuz Mob1bGt(CC0690)Wtsi/Mob1bGt(CC0690)Wtsi Tg(Alb-cre)21Mgn mice
• not as much as in Mob1atm1.1Asuz/Mob1atm1.1Asuz Mob1bGt(CC0690)Wtsi/Mob1bGt(CC0690)Wtsi Tg(Alb-cre)21Mgn mice
• not as much as in Mob1atm1.1Asuz/Mob1atm1.1Asuz Mob1bGt(CC0690)Wtsi/Mob1bGt(CC0690)Wtsi Tg(Alb-cre)21Mgn mice

endocrine/exocrine glands
• increased immature cholangiocyte-like and oval cells but not as much as in Mob1atm1.1Asuz/Mob1atm1.1Asuz Mob1bGt(CC0690)Wtsi/Mob1bGt(CC0690)Wtsi Tg(Alb-cre)21Mgn mice




Genotype
MGI:5897811
cn55
Allelic
Composition
Mob1atm1.1Asuz/Mob1atm1.1Asuz
Mob1bGt(CC0690)Wtsi/Mob1bGt(CC0690)Wtsi
Wwtr1tm1Hku/Wwtr1tm1Hku
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * DBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Mob1atm1.1Asuz mutation (0 available); any Mob1a mutation (8 available)
Mob1bGt(CC0690)Wtsi mutation (0 available); any Mob1b mutation (3 available)
Speer6-ps1Tg(Alb-cre)21Mgn mutation (5 available); any Speer6-ps1 mutation (2 available)
Wwtr1tm1Hku mutation (0 available); any Wwtr1 mutation (8 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
liver/biliary system
• increased immature cholangiocyte-like and oval cells but not as much as in Mob1atm1.1Asuz/Mob1atm1.1Asuz Mob1bGt(CC0690)Wtsi/Mob1bGt(CC0690)Wtsi Tg(Alb-cre)21Mgn mice
• not as much as in Mob1atm1.1Asuz/Mob1atm1.1Asuz Mob1bGt(CC0690)Wtsi/Mob1bGt(CC0690)Wtsi Tg(Alb-cre)21Mgn mice
• not as much as in Mob1atm1.1Asuz/Mob1atm1.1Asuz Mob1bGt(CC0690)Wtsi/Mob1bGt(CC0690)Wtsi Tg(Alb-cre)21Mgn mice

endocrine/exocrine glands
• increased immature cholangiocyte-like and oval cells but not as much as in Mob1atm1.1Asuz/Mob1atm1.1Asuz Mob1bGt(CC0690)Wtsi/Mob1bGt(CC0690)Wtsi Tg(Alb-cre)21Mgn mice




Genotype
MGI:5444453
cn56
Allelic
Composition
Hsd11b1tm1Ggla/Hsd11b1tm1Ggla
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * DBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hsd11b1tm1Ggla mutation (0 available); any Hsd11b1 mutation (28 available)
Speer6-ps1Tg(Alb-cre)21Mgn mutation (5 available); any Speer6-ps1 mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
N
• when fed a high fat diet, mice exhibit normal insulin resistance
• mice fed a high fat diet exhibit normal hepatic lipid accumulation
• mice fed a high fat diet exhibit less of an increase in insulin levels compared with control mice
• when fed a low fat diet
• however, there is no significant difference when mice are fed a high fat diet
• mice fed a high fat diet resist glucose intolerance with enhanced glucose clearance compared with control mice

behavior/neurological
• marginally reduced when fed normal chow

endocrine/exocrine glands

growth/size/body